This action might not be possible to undo. Are you sure you want to continue?
PDQ ORAL DISEASE
Actinic (Solar) Cheilitis
Etiology • Chronic, excessive exposure to solar radiation; ultraviolet spectrum (ranging from 290 to 320 nm) most damaging • Fair-complexioned people more severely affected than others • May progress to cutaneous actinic keratosis and/or squamous cell carcinoma Clinical Presentation • Vermilion portion of lower lip • Pale irregularly opaque (keratotic) surface with intervening red (atrophic) zones • Obfuscated to effaced cutaneous-vermilion border • More advanced lesions are scaly, crusted and/or indurated. • Progression to carcinoma often heralded by persistent ulceration or erosion Microscopic Findings • Hyperkeratosis • Epithelial atrophy • Variable degrees of epithelial dysplasia • Amphophilic to basophilic change in submucosa (elastosis) • Telangiectasia Diagnosis • Thermal/chemical burn ruled out by history • Chronic ultraviolet light exposure • Biopsy findings Differential Diagnosis • Exfoliative cheilitis • Squamous cell carcinoma
Treatment • Prevention of further damage with sunscreens blocking longwave ultraviolet A (UVA) and short-wave ultraviolet B (UVB) light • Biopsy of clinically suspicious areas • CO2 laser vermilionectomy • Topical 5-fluorouracil or vermilionectomy for severe disease • Excision or resection-reconstruction if malignant transformation has occurred Prognosis • Lifelong follow-up • Up to 10% develop into squamous cell carcinoma. • When carcinoma develops, growth tends to be slow and metastasis occurs late; 85 to 90% long-term survival
PDQ ORAL DISEASE
Etiology • Infection with a fungal organism of the Candida species, usually Candida albicans • Associated with predisposing factors: most commonly, immunosuppression, diabetes mellitus, antibiotic use, or xerostomia (due to lack of protective effects of saliva) Clinical Presentation • Acute (thrush) • Pseudomembranous • Painful white plaques representing fungal colonies on inflamed mucosa • Erythematous (acute atrophic): painful red patches caused by acute Candida overgrowth and subsequent stripping of those colonies from mucosa • Chronic • Atrophic (erythematous): painful red patches; organism difficult to identify by culture, smear, and biopsy • “Denture-sore mouth”: a form of atrophic candidiasis associated with poorly fitting dentures; mucosa is red and painful on denture-bearing surface • Median rhomboid glossitis: a form of hyperplastic candidiasis seen on midline dorsum of tongue anterior to circumvallate papillae • Perlèche: chronic Candida infection of labial commissures; often co-infected with Staphylococcus aureus • Hyperplastic/chronic hyperplastic: a form of hyperkeratosis in which Candida has been identified; usually buccal mucosa near commissures; cause and effect not yet proven • Syndrome associated: chronic candidiasis may be seen in association with endocrinopathies Diagnosis • Microscopic evaluation of lesion smears • Potassium hydroxide preparation to demonstrate hyphae • Periodic acid–Schiff (PAS) stain • Culture on proper medium (Sabouraud’s, corn meal, or potato agar) • Biopsy with PAS, Gomori’s methenamine silver (GMS), or other fungal stain of microscopic sections
Differential Diagnosis • Allergic or irritant contact stomatitis • Atrophic lichen planus Treatment • Topical or systemic antifungal agents • For immunocompromised patients: routine topical agents after control of infection is achieved, usually with systemic azole agents • See “Therapeutics” section • Correction of predisposing factor, if possible • Some cases of chronic candidiasis may require prolonged therapy (weeks to months). Prognosis • Excellent in the immunocompetent host
PDQ ORAL DISEASE
Etiology • Causes may be atopic, contact, factitious, infectious, systemic, or medication induced. Clinical Presentation • Usually involves lower lip (in both genders); can involve both lips • Tender or asymptomatic crusts and impacted scale of vermilion • Minimal inflammation Diagnosis • Clinical appearance • Nonspecific microscopy results Differential Diagnosis • Atopic cheilitis • Actinic cheilitis • Contact cheilitis Treatment • Determination of cause • Supportive care • Topical or intralesional corticosteroids, including lip ointments/ pomade (hypoallergenic) • Topical tacrolimus ointment Prognosis • Chronic • Psychologic support for factitial cheilitis
PDQ ORAL DISEASE
Etiology • Ectopic sebaceous glands within the oral mucosa and vermilion portion of the lips Clinical Presentation • Multiple, scattered, yellowish pink, maculopapular granules • Buccal mucosa and vermilion of lips predominantly affected • Asymptomatic • Increasingly prominent after puberty Diagnosis • Bilateral distribution and appearance • Lack of symptoms • If biopsy performed, normal sebaceous glands in the absence of hair follicles noted Differential Diagnosis • Candidiasis Treatment • None • Reassurance Prognosis • Excellent
White Lesions 9 .
may be familial • May be related to atopy • Small percentage associated with cutaneous psoriasis Clinical Presentation • May be symptomatic in association with spicy or acidic foods • Focal red depapillated areas bordered by slightly elevated. if symptomatic Prognosis • Excellent • No malignant potential • May last months to years with periods of remission . size.10 PDQ ORAL DISEASE Geographic Tongue Etiology • Unknown. yellowish margin • Dynamic behavior: changes in shape. intensity day to day • Dorsal and lateral tongue surfaces affected predominantly • Ventral tongue and other areas less often involved • Often associated with fissured tongue Diagnosis • Location and appearance • Biopsy confirmation usually unnecessary Differential Diagnosis • Reiter’s syndrome • Lichen planus • Lupus erythematosus • Candidiasis • Psoriasis Treatment • None. if asymptomatic • Topical corticosteroids.
White Lesions 11 .
12 PDQ ORAL DISEASE Hairy Leukoplakia Etiology • Probably due to opportunistic Epstein-Barr virus (EBV) infection of epithelial cells • Usually in an immunocompromised or immunosuppressed host Clinical Presentation • Usually arises on lateral tongue border • Early lesions are fine. white. predisposing condition to be investigated • Can be suppressed with acyclovir for esthetics • Antiviral acyclovir • Podophyllin resin topically Prognosis • May herald human immunodeficiency virus (HIV) disease in vast majority of cases • Also may be present after AIDS is established . vertical streaks with an overall corrugated surface • Later lesions may be thickened to be plaque-like • Extensive lesions can involve dorsum of tongue and buccal mucosa • May serve as a pre-AIDS (acquired immunodeficiency syndrome) sign Diagnosis • Incisional biopsy findings show characteristic EBV nuclear inclusions in upper-level keratinocytes Differential Diagnosis • Frictional hyperkeratosis • Lichen planus • Hyperplastic candidiasis Treatment • None necessary.
White Lesions 13 .
radiation therapy. 5 to 15 strokes. or use of oxygenating mouth rinses (H2O2. heavy smoking. systemic or topical antibiotic therapy. xerostomia. hyperkeratotic filiform papillae on tongue dorsum producing a “furred” to “hairy” texture • Color varies from tan to brownish yellow to black depending upon diet. soft diet. once or twice daily) • Topical podophyllin (5% in benzoin) followed by débridement • Elimination of cause. sodium perborate) Clinical Presentation • Elongated.14 PDQ ORAL DISEASE Hairy Tongue Etiology • Generally unknown • May be related to poor oral hygiene. chromogenic organisms • Symptoms usually minimal. drugs. may produce gagging or tickling sensation on palate Diagnosis • Clinical features • Culture or cytologic studies not helpful Treatment • Physical débridement (brushing with a soft-bristled toothbrush. if identified Prognosis • Excellent .
White Lesions 15 .
common in general population. no relation to dysplasia/carcinoma • Reassurance Prognosis • Excellent . • Individual cells with clear cytoplasm and compact nuclei • Normal basal cell layer Differential Diagnosis • Cheek chewing • Hereditary benign intraepithelial dyskeratosis • White sponge nevus • Lichen planus • Candidiasis Treatment • None necessary. with racial clustering in Blacks Clinical Presentation • Symmetric. • Biopsy findings will show marked intracellular edema of spinous layer.16 PDQ ORAL DISEASE Leukoedema Etiology • Unknown • Benign. asymptomatic • Buccal mucosa involved by gray-white. milky surface with an opalescent quality • Wrinkled surface features at rest • Dissipation of changes with stretching of mucosa Diagnosis • Clinical recognition is sufficient. diffuse.
White Lesions 17 .
Clinical Presentation • An idiopathic white (sometimes white-and-red) patch • Most common on lip. cryosurgery) • Option to observe lesions diagnosed as benign hyperkeratosis or mild dysplasia . vitamin A) and infection (Candida albicans. verrucous.18 PDQ ORAL DISEASE Leukoplakia Etiology • Essentially unknown. although many cases related to use of tobacco or areca nut in its various formulations • Other possible factors include nutritional deficiency (iron. floor of mouth. gingiva. vermilion portion of lip • Clinical subsets include homogeneous. Differential Diagnosis • Other white lesions • Frictional keratosis • Hyperplastic candidiasis • Burn (thermal/chemical) • Lichen planus • Genetic alterations (genodermatoses) • White sponge nevus • Hereditary benign intra• Dyskeratosis epithelial dyskeratosis Treatment • Excision modalities (surgery. speckled. human papillomavirus). and proliferative verrucous leukoplakia (proliferative form may be multiple and persistent) • Cases may advance or regress unpredictably—reflective of a dynamic process • Most occur in the fifth decade and beyond • Progress to dysplasia or malignancy may occur with little or no change in clinical appearance. laser ablation. Diagnosis • Performance of a biopsy is mandatory after elimination of any suspected causative factors • Multiple biopsies of large lesions are needed to be performed due to microscopic heterogeneity within a single lesion. buccal mucosa • Increased risk of dysplasia or carcinoma when occurring on tongue.
• Possible dietary measures .White Lesions 19 • Possibly photodynamic therapy • Topical cytotoxic drugs (bleomycin) remain experimental. • Recurrences common following apparent complete excision Prognosis • Guarded • Observation with repeat biopsies to be performed Prevention • Elimination of tobacco use and heavy alcohol consumption • Recurrences may be reduced by systemic retinoid therapy.
angiotensinconverting enzyme inhibitors. other metals Clinical Presentation • White striae or papules. • Most often in buccal mucosa and attached gingiva. antimalarials. sulfonylurea compounds • Contact hypersensitivity • Idiopathic reaction to dental restorations including amalgam. gold. gold. nonsteroidal anti-inflammatory drugs. but any site may be involved Diagnosis • Identification and elimination of causative substance • Biopsy of areas unresponsive to elimination strategy to demonstrate characteristic keratosis and interface inflammation and associated changes • Patch testing performed to confirm contact allergens Differential Diagnosis • Lichen planus • Leukoplakia • Dysplasia/carcinoma Treatment • Alternative drugs or material to be chosen • Topical corticosteroid applications • Topical tacrolimus applications Prognosis • Good • Observation while lesions exist . as with lichen planus • Lesions may appear ulcerative with associated tenderness or pain.20 PDQ ORAL DISEASE Lichenoid Drug Eruptions Etiology • Hypersensitivity to drugs including sulfasalazine. β-blockers. composites.
White Lesions 21 .
papular. atrophic. then gingiva. certain drugs. GVHD to be ruled out • Biopsy • Direct immunofluorescence–fibrinogen and cytoid bodies at interface help confirm Differential Diagnosis • Lichenoid drug eruptions • Erythema multiforme • Lupus erythematosus • Contact stomatitis • Mucous membrane pemphigoid .22 PDQ ORAL DISEASE Lichen Planus Etiology • Unknown • Autoimmune T cell–mediated disease targeting basal keratinocytes (antigen unknown) • Lichenoid changes associated with galvanism. bullous (rare) • Bilateral and often symmetric distribution • Oral site frequency: buccal mucosa (most frequent). genitalia • Negative ocular mucosa history. then lips (least frequent) • Skin sites: forearm. then tongue. no history of blistering • Use of drugs. 50% also have oral lesions (25% with oral lesions have concomitant skin lesions) • White females (60%) • Occurs in fourth to eighth decades • Variants: reticular (most common oral form).5 to 1% of population have cutaneous lichen planus. scalp. genitalia Microscopic Findings • Hyperkeratosis • Basal keratinocyte necrosis • Lymphocytes at epithelial-connective tissue interface Diagnosis • Examination of oral mucosa. plaque types. erosive (painful). shin. galvanism. skin. graft-versus-host disease (GVHD). contact allergens Clinical Presentation • Up to 3 to 4% of population have oral lichen planus • 0.
may last for years/decades • Tends to be chronic . rare malignant transformation (0. can be expected. • Good prognosis.5–3%) • May be cyclic.White Lesions 23 Treatment of Oral Lichen Planus • Mild to moderate: topical corticosteroids • Severe: systemic immunosuppression. chiefly with prednisone • Corticosteroid-sparing drugs with prednisone • Topical tacrolimus ointment Prognosis • Control. not cure.
keratotic surface • Surface often appears granular to macerated • More uniform keratotic surface may develop over time if habit continues • Most common sites are lip and buccal mucosa Microscopic Findings • Very irregular. white. low-grade biting habit Clinical Presentation • Shaggy.24 PDQ ORAL DISEASE Morsicatio Buccarum/Labiorum (Cheek and Lip Chewing) Etiology • Chronic. fimbriated surface keratin • Surface bacterial colonization • No connective tissue changes Diagnosis • Presentation • Biopsy Differential Diagnosis • Leukoedema • Leukoplakia • Lichen planus • Lichenoid tissue reactions Treatment • Elimination of hyperfunction habit Prognosis • Excellent .
White Lesions 25 .
clinical course.26 PDQ ORAL DISEASE Proliferative Verrucous Leukoplakia Etiology • Some associated with human papillomavirus types 16 and 18 • Role of tobacco and other risk factors • Represents a clinicopathologic spectrum of disease • Multiple lesions develop from hyperkeratosis and/or verrucous hyperplasia to verrucous carcinoma or papillary squamous cell carcinoma Clinical Presentation • Slowly progressive and persistent • Initially a flat hyperkeratotic to warty surface • Surface may be friable • Typically multiple and recurrent • Seen in middle-aged to elderly patients Diagnosis • Based upon appearance. and microscopic diagnosis (ie. clinical-pathologic correlation) • Microscopic diagnoses include epithelial hyperplasia. “atypical papillary-verrucal proliferation.” verrucous or well-differentiated squamous cell carcinoma Differential Diagnosis • Idiopathic leukoplakia • Oral warts/condyloma • Verrucous/squamous cell carcinoma Treatment • Surgical excision • Mucosal stripping or excision for benign lesions • Wide excision to resection for advanced lesions • Laser ablation for benign/atypical lesions • Systemic retinoids to control keratosis . verrucous hyperplasia. hyperkeratosis.
• Fair to good prognosis after malignant transformation • Frequent follow-up visits recommended and surgical intervention as new/recurrent lesions develop . usually many years after initial lesion(s) develops.White Lesions 27 Prognosis • Progression to carcinoma frequently occurs.
stripping of mucosal site Prognosis • Generally good with tobacco cessation • Malignant transformation to squamous cell carcinoma or verrucous carcinoma occurs but less frequently than does smokingrelated carcinoma. Diagnosis • Clinical appearance • Biopsy Differential Diagnosis • Leukoplakia (idiopathic) • Mucosal burn (chemical/thermal) Treatment • Discontinuation of habit • If dysplasia is present. white.28 PDQ ORAL DISEASE Smokeless Tobacco Keratosis (Snuff Pouch) Etiology • Persistent habit of holding ground tobacco within the mucobuccal vestibule Clinical Presentation • Usually in men in Western countries • Powdered snuff use prevalent in Southeast United States often by women • Mucosal pouch with soft. . fissured appearance • Surface may be pumice-like to verrucous • Leathery surface due to chronic tobacco use over many years Microscopic Findings • Hyperkeratosis with parakeratotic “chevron sign” at surface • Increased vascularity • Older lesions with hyalinization in submucosa and minor salivary glands • Epithelial dysplasia and carcinoma may evolve.
White Lesions 29 .
burning. alkaloids and tannin in the areca nut are liberated by action of slaked lime within the quid. and other ingredients. which is wrapped with the betel leaf • Risk of oral squamous cell carcinoma is increased several-fold Clinical Presentation • Early phase: tenderness. hyperkeratosis • Epithelial dysplasia found in up to 15% of cases Diagnosis • Appearance • History Differential Diagnosis • Lichen sclerosus Treatment • Intralesional corticosteroid placement • Surgical release of scar bands in latter stages • Careful follow-up and vigilance for development of squamous cell carcinoma Prognosis • Irreversible • Fair . trismus • Sites most often affected: buccal mucosa. melanosis • Later phase: mucosal rigidity. vesicles. tobacco.30 PDQ ORAL DISEASE Submucous Fibrosis Etiology • Results from direct mucosal contact with a quid containing areca (betel) nut. • Epithelial thinning. soft palate Microscopic Findings • Biopsy results show submucosal deposition of dense collagen. soft palate • Leukoplakia of surface with pallor • Deep scarring. epithelial atrophy in cheeks. erythema.
White Lesions 31 Both photographs courtesy of Dr. . Greenspan. John S.
intracellular edema • Perinuclear condensation of keratin Diagnosis • Clinical appearance • Family history • Microscopic findings Differential Diagnosis • Idiopathic leukoplakia • Chemical/thermal burn • Chronic low-grade trauma (morsicatio) Treatment • None required • No malignant potential Prognosis • Excellent . thickened. acanthosis. white mucosa • Buccal mucosa chiefly affected • No functional impairment • Increased prominence during second decade Microscopic Findings • Parakeratosis. esophageal.32 PDQ ORAL DISEASE White Sponge Nevus Etiology • Hereditary (autosomal-dominant) disorder of keratinization affecting nonkeratinizing oral. and anogenital mucosal epithelium • Point mutations in the keratin 4 and/or 13 genes Clinical Presentation • Asymptomatic • Deeply folded.
White Lesions 33 .
hemophilia • Vascular wall defects • Coagulopathy • Trauma Clinical Presentation • Larger than pinpoint spots (ie. leukemia. Kaposi’s sarcoma. thrombocytopenia.34 PDQ ORAL DISEASE Red/Blue Lesions Ecchymosis Etiology • Soft tissue hemorrhage • Blood dyscrasia with secondary thrombocytopenia. von Willebrand’s disease. trauma Treatment • Identification of etiology. larger than petechiae) • Nonvesicular. macular surface • Lesions do not blanch with pressure • Red to reddish blue to brown color Diagnosis • Characteristic size. color • History • Blood count. and corresponding treatment Prognosis • Excellent . coagulation profile Differential Diagnosis • Hemophilia. hemangioma.
Red/Blue Lesions 35 .
retromolar trigone area. well-defined patch(es) • Most common on floor of mouth. often velvety. history of tobacco/alcohol use • Biopsy results differentiate from inflammatory and atrophic lesions Differential Diagnosis • Erythematous (atrophic) candidiasis • Kaposi’s sarcoma • Ecchymosis • Contact stomatitis • Vascular malformation • Squamous cell carcinoma • Geographic tongue/erythema migrans Treatment • Surgical excision if proven dysplastic/malignant Prognosis • Fair to good depending upon microscopic diagnosis • Almost all cases are premalignant to malignant upon initial discovery. lateral tongue • Usually asymptomatic • May be smooth to nodular • Chiefly in males Diagnosis • Appearance.36 PDQ ORAL DISEASE Erythroplakia Etiology • Unknown: a red patch that cannot be clinically attributed to another condition • Contributing factors include tobacco use. alcohol consumption Clinical Presentation • Red. .
Red/Blue Lesions 37 .
may be related to the following: • Secondary candidiasis (antifungal prescription) • Idiopathic factors Treatment • Usually none • With candidal colonization.38 PDQ ORAL DISEASE Fissured Tongue Etiology • Unknown • May be hereditary • Occurs with greater prevalence as population ages Clinical Presentation • Multiple crenations or fissures • May be seen in association with erythema migrans/geographic tongue • Prominence increases with age • Usually asymptomatic • A component of Melkersson-Rosenthal syndrome • May be a source of halitosis Diagnosis • Characteristic appearance • If symptomatic (pain. burning). • Careful débridement with soft-bristled brush. once or twice daily Prognosis • Excellent . topical antifungal preparations are effective. 5 to 15 strokes.
Red/Blue Lesions 39 .
and usually involute over several years. • Malformations generally are persistent. grow rapidly. • Color varies from red to blue depending on depth. and caliber of vessels • Range in size from few millimeters to massive with disfigurement • Most common on lips. Diagnosis • Aspiration • Blanching under pressure (diascopy) • Imaging studies Differential Diagnosis • Purpura • Telangiectasia • Kaposi’s sarcoma • Other vascular neoplasms . grow with the child. and do not involute. mental retardation. buccal mucosa • Usually asymptomatic • Sturge-Weber syndrome (trigeminal encephaloangiomatosis) includes cutaneous vascular malformations (port wine stains) along trigeminal nerve distribution. degree of congestion. tongue.40 PDQ ORAL DISEASE Hemangioma Etiology • Benign developmental anomalies of blood vessels that may be subclassified as congenital hemangiomas and vascular malformations • “Congenital hemangioma” usually noted initially in infancy or childhood (hamartomatous proliferation) • Congenital hemangioma due to proliferation of endothelial cells • “Vascular malformations” due to abnormal morphogenesis of arterial and venous structures Clinical Presentation • Congenital lesions usually arise around time of birth. and seizures.
) • Sclerotherapy • Microembolization followed by resection for large malformations or if bleeding is problematic Prognosis • Guarded . • Surgery (scalpel. laser [argon. cryosurgery.Red/Blue Lesions 41 Treatment • Observation • Congenital hemangiomas typically involute. which are poorly defined. copper])—congenital hemangiomas usually are circumscribed and more easily removed than are vascular malformations. whereas vascular malformations persist. (Vascular malformations are associated with excessive bleeding and recurrence.
which may rupture with associated signs of chronic gastrointestinal blood loss. finger tips • Commonly associated with epistaxis due to involvement of nasal mucosa • Increase in number and prominence with age • Blanch under pressure (diascopy positive) • Lesions can affect gastrointestinal mucosa. macular to slightly papular red lesions of skin and mucosa • Most common on lips. tongue. • Arteriovenous (eg. buccal mucosa.42 PDQ ORAL DISEASE Hereditary Hemorrhagic Telangiectasia (Rendu-Osler-Weber Syndrome) Etiology • Not uncommon. esophageal dysfunction. may produce anemia Diagnosis • Family history • Distribution of lesions Differential Diagnosis • CREST syndrome (calcinosis cutis. telangiectasia) • Chronic hepatitis • Radiation-induced vascular alterations Treatment • Observation • Monitoring of pulmonary lesions. embolization if indicated Prognosis • Lifelong follow-up/monitoring • 4 to 10% death rate from complications of the disease . Raynaud’s phenomenon. sclerodactyly. familial (autosomal-dominant) mucocutaneous vascular disease • Some cases may be nonfamilial (spontaneous mutation). Clinical Presentation • Multifocal. pulmonary) malformations also can occur.
Red/Blue Lesions 43 .
buccal mucosa. oral lesions rarely seen • AIDS-associated KS most commonly seen on keratinized mucosa/mucoperiosteal tissues.44 PDQ ORAL DISEASE Kaposi’s Sarcoma Etiology • Several forms • Classic idiopathic form affecting extremeties • Endemic form (African) • Immunosuppression-associated form • Acquired immunodeficiency syndrome (AIDS)-associated form • All forms. strong predilection for hard palate. extravascular red blood cells Differential Diagnosis • Hematoma • Hemangioma • Ecchymosis • Malignant melanoma • Pyogenic granuloma • Amalgam tattoo . oral lesions rarely seen • Endemic form more rapid. especially AIDS-associated and immunosuppressionassociated forms. and tongue (prevalence decreasing with treatment for AIDS) • Evolution from bluish macule to nodule(s) • Evolution to multiple lesions • May precede or follow cutaneous lesions • Usually asymptomatic Diagnosis • Location and appearance • May occur in up to one-third of AIDS patients • Biopsy showing spindle cell proliferation with vascular slits. followed by gingiva. may be caused by or closely related to a herpesvirus (human herpesvirus 8 [HHV-8] or Kaposi’s sarcoma–associated herpesvirus [KSHV]). Clinical Presentation • Classic form associated with slow but pernicious growth over many years.
sclerosing agents (sodium morrhuate) • Systemic chemotherapy: interferon-α. bleomycin. daunorubicin • Most treatment is palliatively directed.Red/Blue Lesions 45 Treatment of AIDS-Associated Form • Radiation therapy: single fraction or equivalent fractionated therapy of 800 cGy • Intralesional therapy: interferon-α. vincristine. vinblastine. vinblastine (2 mg/cc). Prognosis • Variable. vincristine. depending upon host’s immune status. but generally poor in AIDS-associated form .
determination of underlying cause Differential Diagnosis • See “Etiology” Treatment • None. depending upon etiology . measles).46 PDQ ORAL DISEASE Petechiae Etiology • Viral infection (Epstein-Barr virus [EBV]-mononucleosis. frequent vomiting. fellatio. giving birth. rickettsial infection • Thrombocytopenia. leukemia • Disseminated intravascular coagulation (DIC) • Trauma: prolonged coughing. observation only Prognosis • Variable. violent Valsalva maneuvers Clinical Presentation • Pinpoint hemorrhage into mucosa/submucosa • Asymptomatic • Usually involves the soft palate • No blanching on pressure (diascopy) Diagnosis • Clinical features • History.
Red/Blue Lesions 47 .
velvety gingival surface • Surface epithelium becomes nonkeratinized. • Limited to attached gingiva Diagnosis • Response to elimination of possible etiologic agents • Biopsy results show plasma cell infiltration within the submucosa and lamina propria beneath an acanthotic epithelium.48 PDQ ORAL DISEASE Plasma Cell Gingivitis Etiology • Usually represents a hypersensitivity phenomenon to an agent such as the following: • Cinnamon/cinnamon flavoring • Candy flavors • Toothpaste/mouthwash • Plaque antigens Clinical Presentation • Reddened. • Patch testing Differential Diagnosis • Lupus erythematosus • Wegener’s granulomatosis • Chronic candidiasis • Lichen planus • Mucous membrane pemphigoid Treatment • Elimination of causative factor Prognosis • Reversal with removal of causative agent .
Red/Blue Lesions 49 .
calculus or foreign body) • Misnomer—neither pyogenic nor granulomatous Clinical Presentation • Occurs at any age. especially if ulcerated Diagnosis • History of gradual to rapid onset • Identification of a stimulus or causative factor (eg. but usually in children. persistent trauma or irritation (eg. physical irritant) • Histologic evaluation Differential Diagnosis • Peripheral giant cell granuloma • Peripheral ossifying fibroma • Metastatic tumor • Kaposi’s sarcoma • Vascular malformation .50 PDQ ORAL DISEASE Pyogenic Granuloma Etiology • A reactive hyperplasia of capillaries and fibroblasts • Related to chronic. and women • Red. young adults. • Sessile to pedunculated commonly on gingiva. a yellow fibrinous exudate covers the lesion. trauma. lower lip. but also on areas that are traumatized (eg. lobular to smoothly contoured appearance • When ulcerated. buccal mucosa) • Bleeds easily but is painless Microscopic Findings • Hyperplastic granulation tissue • Often lobular aggregation of proliferative vascular tissue • Acute and chronic inflammation may be present.
Red/Blue Lesions 51 Treatment • Local excision. scalpel excision • Laser ablation • Electrosurgery • If on gingiva. excision should be extended to the periosteum or periodontal ligament Prognosis • Excellent • Recurrence occasional .
sublingual regions • Blanches with compression (diascopy) • May become thrombosed Diagnosis • Clinical appearance • Histologic viewing of large-caliber. ultraviolet light) • Occur with increasing frequency over 40 years of age Clinical Presentation • Blue.52 PDQ ORAL DISEASE Varices Etiology • An abnormal venous dilatation • Congenital or from damage to vessel wall (trauma. or laser ablation Prognosis • Excellent . sclerotherapy. evolves slowly • Common on lower lip. if stable • Elimination by excision. thin-walled vein Differential Diagnosis • Mucocele • Vascular neoplasm • Blue rubber bleb nevus syndrome • Hereditary hemorrhagic telangiectasia (Rendu-Osler-Weber syndrome) Treatment • Observation only. lobulated surface • Painless.
Red/Blue Lesions 53 .
but it may be severely blistered. reduction of oral opening. depending upon the specific form of many subtypes recognized • Mucosal lesions range in severity from mild to debilitating. with increased risk for squamous cell carcinoma development. ankyloglossia • Scarring can be associated with atrophy and leukoplakia. dermolytic) also demonstrating enamel hypoplasia and caries • Acquisita form with mucous membrane pemphigoid variant shows oral and conjunctival erosions/blisters • Mucosal involvement absent in several variants • Scarring and stricture formation common in severe recessive forms • Mucosa is often friable. depending on subtype: • Inherited forms have wide range of oral mucosal involvement. • Obliteration of vestibules.54 PDQ ORAL DISEASE Vesiculobullous Diseases Epidermolysis Bullosa Etiology • A diverse group of predominantly cutaneous. mechanobullous diseases • Inherited form: autosomal dominant or recessive patterns may occur • Acquired form (acquisita): autoimmune from autoantibodies (immunoglobulin G [IgG]) to type VII collagen deposited within the basement membrane zone and upper dermis or lamina propria Clinical Presentation • Variable. . but also mucosal. • Loss of oral anatomic landmarks may follow severe scarring (eg. eroded. with most severe form (autosomal recessive. or ulcerated. tongue mucosa may become smooth and atrophic with episodes of blistering and scarring).
Vesiculobullous Diseases 55 Microscopic Findings • Bullae vary in location depending upon the form that is present: • Intraepithelial in nonscarring forms • At epithelial–connective tissue junction in dystrophic forms • Subepithelial/intradermal in scarring forms • Ultrastructural findings are as follows: • Intraepithelial forms associated with defective cytokeratin groups • Junctional forms associated with defective anchoring filaments at hemidesmosomal sites (epithelial–connective tissue junction) • Dermal types demonstrate anchoring fibril or collagen destruction. Diagnosis • Distribution of lesions • Family history • Microscopic evaluation • Ultrastructural evaluation • Immunohistochemical evaluation of basement membrane zone using specific labeled antibodies as markers for site of blister formation Differential Diagnosis • Varies with specific form • Generally includes the following: • Bullous pemphigoid • Mucous membrane (cicatricial) pemphigoid • Erosive lichen planus • Dermatitis herpetiformis • Porphyria cutanea tarda • Erythema multiforme • Bullous impetigo • Kindler syndrome • Ritter’s disease (continued) .
daily topical fluoride applications. and cyclosporine may be effective • Acquisita and inherited forms: • Avoidance of trauma • Dental prevention strategies including extra-soft brushes.56 PDQ ORAL DISEASE Treatment • Acquisita form: • Some recent success with colchicine and dapsone • Immunosuppressive agents including azathioprine. methotrexate. dietary counseling Prognosis • Widely variable depending on subtype .
Vesiculobullous Diseases 57 .
crusted. and hemorrhagic lesions (serosanguinous exudate) known as Stevens-Johnson syndrome when severe • Predilection for young adults • As many as one-half of oral cases have associated erythematous to bullous skin lesions. analgesics. phenolphthalein-containing laxatives. including sulfonamides. • Target or iris skin lesions may be noted over extremities. shallow ulcers and erosions with irregular margins • Early mucosal lesions are macular. • Genital and ocular lesions may occur. 2. and occasionally bullous. possibly related to circulating immune complexes Clinical Presentation • Acute onset of multiple.58 PDQ ORAL DISEASE Erythema Multiforme Etiology • Many cases preceded by infection with herpes simplex. • May affect oral mucosa and skin synchronously or metachronously • Lips most commonly affected with eroded. other antibiotics. Diagnosis • Appearance • Rapid onset • Multiple site involvement in one-half of cases • Biopsy results often helpful. • Usually self-limiting. erythematous. less often with Mycoplasma pneumoniae or other organisms • May be related to drug consumption. barbiturates • Another trigger may be radiation therapy. painful. but not always diagnostic Differential Diagnosis • Viral infection. in particular.to 4-week course • Recurrence is common. acute herpetic gingivostomatitis (Note: Erythema multiforme rarely affects the gingiva.) . • Essentially an immunologically mediated reactive process.
Prognosis • Generally excellent • Recurrences common . antipyretics • If evidence of an antecedent viral infection or trigger exists. topical corticosteroid agents • Severe (major) form: systemic corticosteroids. • See “Therapeutics” section for details. liquid diet.Vesiculobullous Diseases 59 • • • • Pemphigus vulgaris Major aphthous ulcers Erosive lichen planus Mucous membrane (cicatricial) pemphigoid Treatment • Mild (minor) form: symptomatic/supportive treatment with adequate hydration. analgesics. systemic antiviral drugs during the disease or as a prophylactic measure may help. parenteral fluid replacement.
Prognosis • Excellent • Lifelong immunity. floor of mouth. and digital lesions are deeply seated. and erythematous • Short course with mild symptoms Diagnosis • Concomitant oral and cutaneous lesions • Skin lesions commonly involve hands and feet.60 PDQ ORAL DISEASE Hand-Foot-and-Mouth Disease Etiology • A very common enterovirus infection (coxsackievirus A10 or A16). usually less than 1 week Clinical Presentation • Oral mucosal lesions with focal herpes simplex–like appearance. vesicular. chiefly in children • Incubation period is short. • Skin lesions may involve buttocks. plantar. • Antibody-titer increase measured between acute and recovery phases Differential Diagnosis • Herpangina • Herpes simplex infection • Acute lymphonodular pharyngitis Treatment • Symptomatic treatment only • Patient should be cautioned against the use of aspirin to manage fever. usually involving nonkeratinized tissue (soft palate. which may occur in mild epidemic proportion. but it is strain specific . labial-buccal mucosa) • Accompanying palmar.
Vesiculobullous Diseases 61 .
malaise. usually occurs in summer • Often subclinical • Posterior oral cavity. headache. and vomiting • Self-limiting course. time of year. 10. and 16) or group B (1–5) • Occasionally due to echovirus 9 or 17 Clinical Presentation • Incubation period of 5 to 9 days • Acute onset • Usually endemic in young children. contact with known infected individual Differential Diagnosis • Hand-foot-and-mouth disease • Varicella • Acute herpetic gingivostomatitis Treatment • Soft diet • Hydration • Antipyretics • Chlorhexidine rinses • Compounded mouth rinses Prognosis • Excellent . dysphagia. lymphadenitis.62 PDQ ORAL DISEASE Herpangina Etiology • Most often by members of coxsackievirus group A (7. fever. 9. location of lesions. tonsillar pillars involved • Macular erythematous areas precede short-lived vesicular eruption. usually under 2 weeks Diagnosis • Other viral illnesses to be ruled out or separated • Course. followed by superficial ulceration • Accompanied by pharyngitis.
Vesiculobullous Diseases 63 .
pain. perioral skin may be involved • 7. fibrinous base with an erythematous halo • Both keratinized and nonkeratinized mucosa affected • Gingival tissue with edema. in addition to oral ulcers • Coalescing.to 14-day course Diagnosis • Usually by clinical presentation and pattern of involvement • Cytology preparation to demonstrate multinucleate virusinfected giant epithelial cells • Biopsy results of intact macular area show intraepithelial vesicles or early virus-induced epithelial (cytopathic) changes • Viral culture or polymerase chain reaction (PCR) examination of blister fluid or scraping from base of erosion Differential Diagnosis • Herpangina • Hand-foot-and-mouth disease • Varicella • Herpes zoster (shingles) • Erythema multiforme (typically no gingival lesions) . • Incubation period of up to 2 weeks • Abrupt onset in those with low or absent antibody to HSV-1 • Fever. pinhead-sized vesicles that ulcerate • Ulcers show a yellow. intense erythema. grouped. anorexia. lymphadenopathy. and tenderness • Lips.5 and 5 years of age. headache.64 PDQ ORAL DISEASE Herpetic Stomatitis: Primary Etiology • Herpes simplex virus (HSV) • Over 95% of oral primary herpes due to HSV-1 • Physical contact is mode of transmission Clinical Presentation • 88% of population experience subclinical infection or mild transient symptoms • Most cases occur in those between 0.
valacyclovir) if early in course or in immunocompromised patients • Compounded mouth rinse Prognosis • Excellent in immunocompetent host • Remission/latent phase in nearly all those affected who have adequate antibody titers .Vesiculobullous Diseases 65 Treatment • Soft diet and hydration • Antipyretics (avoid aspirin) • Chlorhexidine rinses • Systemic antiviral agents (acyclovir.
66 PDQ ORAL DISEASE Impetigo Etiology • Cutaneous bacterial infection: Streptococcus and Staphylococcus species • Is spread through direct contact • Highly contagious Clinical Presentation • Honey-colored. poststreptococcal glomerulonephritis may develop. β-hemolytic streptococci or group II Staphylococcus aureus) Differential Diagnosis • Herpes simplex (recurrent) • Exfoliative cheilitis • Drug eruptions • Other vesiculobullous diseases Treatment • Topical antibiotics (mupirocin. clindamycin) • Systemic antibiotics Prognosis • Excellent • Rarely. . perioral crusts preceded by vesicles • Flaccid bullae less common (bullous impetigo) Diagnosis • Clinical features • Culture of organism (usually group A.
Vesiculobullous Diseases 67 .
nasopharyngeal. less commonly IgA • Direct immunofluorescence examination positive in 80% of cases • Indirect immunofluorescence examination usually negative • Immunoreactants deposited in lamina lucida in most patients Diagnosis • Biopsy • Direct immunofluorescent examination Differential Diagnosis • Pemphigus vulgaris • Erythema multiforme • Erosive lichen planus • Lupus erythematosus • Epidermolysis bullosa acquisita Treatment • Topical corticosteroids • Systemic prednisone. trigger unknown • Autoantibodies directed against basement membrane zone antigens Clinical Presentation • Vesicles and bullae (short lived) followed by ulceration • Multiple intraoral sites (occasionally gingiva only) • Usually in older adults • 2:1 female predilection • Ocular lesions noted in one-third of cases • Proclivity for scarring in ocular. azathioprine.68 PDQ ORAL DISEASE Mucous Membrane Pemphigoid Etiology • Autoimmune. . laryngeal. and oropharyngeal tissues Microscopic Findings • Subepithelial cleft formation • Linear pattern IgG and complement 3 (C3) along basement membrane zone. or cyclophosphamide • Tetracycline/niacinamide • Dapsone • See “Therapeutics” section for details.
laryngeal. nasopharyngeal. genital) • Management often difficult due to variable response to corticosteroids • Management often requires multiple specialists working in concert (dental. dermatology. otolaryngology) . ocular. ophthalmology.Vesiculobullous Diseases 69 Prognosis • Morbidity related to mucosal scarring (oropharyngeal.
crusted erosive cheilitis • Painful lesions • Cutaneous lesions are polymorphous. may resemble lichen planus. leukemia. and Castleman’s disease Microscopic Findings • Suprabasilar acantholysis. cardiac muscle. and other desmosomal antigens. as well as basement membrane zone antigens Clinical Presentation • Short-lived vesicles and bullae followed by erosion and ulceration.70 PDQ ORAL DISEASE Paraneoplastic Pemphigus Etiology • Autoimmune. and liver may demonstrate paraneoplastic pemphigus antibodies that bind to simple columnar and transitional epithelia Diagnosis • Biopsy of skin or mucosa • Direct immunofluorescent examination of skin or mucosa • Indirect immunofluorescent examination of sera including special substrates . resembles oral pemphigus • Multiple oral sites • Severe hemorrhagic. erythema multiforme. and vacuolar interface inflammation • Direct immunofluorescent testing is positive for epithelial cell surface deposition of IgG and C3 and a lichenoid tissue reaction interface deposition pattern • Indirect immunofluorescent testing is positive for epithelial cell surface IgG antibodies • Special testing with mouse and rat bladder. Waldenström’s macroglobulinemia. desmoplakins I and II. or bullous pemphigoid • Underlying neoplasms such as non-Hodgkin’s lymphoma. keratinocyte necrosis. thymoma. triggered by malignant or benign tumors • Autoantibodies directed against a variety of epidermal antigens including desmogleins 3 and 1. spindle cell neoplasms.
usually fatal. . with malignancies • Management is very challenging.Vesiculobullous Diseases 71 Differential Diagnosis • Pemphigus vulgaris • Erythema multiforme • Stevens-Johnson syndrome • Mucous membrane (cicatricial) pemphigoid • Erosive oral lichen planus Treatment • Identification of concurrent malignancy • Immunosuppressive therapy Prognosis • Good with excision of benign neoplasms • Grave.
ventral tongue) often are initial sites affected • Lateral shearing force on uninvolved skin or mucosa can produce a surface slough or induce vesicle formation (Nikolsky sign) Microscopic Findings • Separation or clefting of suprabasal from basal layer of epithelium • Intact basal layer of surface epithelium • Vesicle forms at site of epithelial split • Nonadherent spinous cells float in blister fluid (Tzanck cells) • Direct immunofluorescence examination positive in all cases • IgG localization to intercellular spaces of epithelium • C3 localization to intercellular spaces in 80% of cases • IgA localization to intercellular spaces in 30% of cases • Indirect immunofluorescence examination positive in 80% of cases • General correlation with severity of clinical disease Diagnosis • Clinical appearance • Mucosal manifestations • Direct/indirect immunofluorescent studies . clinical presentation. shallow irregular ulcers with friable adjacent mucosa • Nonkeratinized sites (buccal. floor.72 PDQ ORAL DISEASE Pemphigus Vulgaris Etiology • An autoimmune disease where antibodies are directed toward the desmosome-related proteins desmoglein 3 or desmoglein 1 • A drug-induced form exists with less specificity in terms of immunologic features. and histopathology Clinical Presentation • Over 50% of cases develop oral lesions as the initial manifestation • Oral lesions develop in 70% of cases • Painful.
mycophenolate mofetil. azathioprine. Prognosis • Guarded • Approximately a 5% mortality rate secondary to long-term systemic corticosteroid–related complications . cyclophosphamide • Plasmapheresis plus immunosuppression • IVIg for some recalcitrant cases • See “Therapeutics” section for details.Vesiculobullous Diseases 73 Differential Diagnosis • Mucous membrane (cicatricial) pemphigoid • Erythema multiforme • Erosive lichen planus • Drug reaction • Paraneoplastic pemphigus Treatment • Systemic immunosuppression • Prednisone.
especially those co-infected with cytomegalovirus. . lesions may occur in any oral site and are more severe (herpetic geometric glossitis). Diagnosis • Characteristic clinical presentation and history • Viral culture or PCR examination of blister fluid or scraping from base of erosion • Cytologic smear • Direct immunofluorescence examination of smear Differential Diagnosis • Erythema multiforme • Herpes zoster (shingles) • Herpangina • Hand-foot-and-mouth disease Treatment • Acyclovir or valacyclovir early in prodrome • Supportive • Acyclovir may be used for prophylaxis for seropositive transplant patients • Ganciclovir may be used for human immunodeficiency virus (HIV)-positive patients. burning.74 PDQ ORAL DISEASE Recurrent Herpetic Stomatitis: Secondary Etiology • Herpes simplex virus • Reactivation of latent virus Clinical Presentation • Prodrome of tingling. or pain at site of recurrence • Multiple. • For recurrent herpes labialis. see “Therapeutics” section. grouped. fragile vesicles that ulcerate and coalesce • Most common on vermilion border of lips or adjacent skin • Intraoral recurrences characteristically on hard palate or attached gingiva (masticatory mucosa) • In immunocompromised patients.
Vesiculobullous Diseases 75 Prognosis • Excellent • Healing without scarring within 10 to 14 days • Protracted healing in HIV-positive patients .
• Genital involvement may occur. drooling • Eye (conjunctival) involvement may occur. • Sometimes referred to as “erythema multiforme major” Clinical Presentation • Labial vermilion and anterior portion of oral cavity usually affected initially • Early phase is macular followed by erosion. and painful ulceration • Lip ulcers appear crusted and hemorrhagic.76 PDQ ORAL DISEASE Stevens-Johnson Syndrome Etiology • A complex mucocutaneous disease affecting two or more mucosal sites simultaneously • Most common trigger: antecedent recurrent herpes simplex infection • Infection with Mycoplasma also may serve as a trigger. • Cutaneous involvement may become bullous. Microscopic Findings • Subepithelial separation with basal cell liquefaction • Intraepithelial neutrophils • Epithelial and connective tissue edema • Perivascular lymphocytic infiltrate Diagnosis • Usually made on clinical grounds • Histopathology is not diagnostic. sialorrhea. • Medications may serve as initiators in some cases. • Iris or target lesions are characteristic on skin. sloughing. foul-smelling presentation as bacterial colonization supervenes • Posterior oral cavity and oropharyngeal involvement leads to odynophagia. Differential Diagnosis • Pemphigus vulgaris • Paraneoplastic pemphigus • Mucous membrane (cicatricial) pemphigoid . • Pseudomembrane.
valacyclovir).Vesiculobullous Diseases 77 • Bullous pemphigoid • Acute herpetic gingivostomatitis • Stomatitis medicamentosa Treatment • Hydration and local symptomatic measures • Topical compounded oral rinses • Systemic corticosteroid use controversial • Recurrent. famciclovir. self-limiting usually • Recurrences not uncommon . virally associated cases may be reduced in frequency with use of daily. • May require admission to hospital burn unit Prognosis • Good. low-dose antiviral prophylactic therapy (acyclovir.
malaise. • Lesions are painful. and pharyngitis with a 2-week incubation • Skin with widespread vesicular eruption • Oral mucosa with short-lived vesicles that rupture forming shallow. grouped vesicular eruption of skin and/or oral mucosa • Vesicles may coalesce prior to ulceration and crusting. dermatomal. defined ulcers • Herpes zoster (shingles) • Unilateral.78 PDQ ORAL DISEASE Varicella and Herpes Zoster Etiology • Primary and recurrent forms due to varicella-zoster virus (VZV) • Primary VZV (chickenpox): a childhood exanthem • Secondary (recurrent) VZV (herpes zoster/shingles) infection: most common in elderly or immunocompromised adults Clinical Presentation • Varicella (chickenpox) • Fever. paresthesia. headache. burning. tingling • Postherpetic pain may be severe. • Prodromal symptoms along affected dermatome may occur. • Pain. Diagnosis • Clinical appearance and symptoms • Cytologic smear with cytopathic effect present (multinucleated giant cells) • Viral culture or PCR examination of blister fluid or scraping from base of erosion • Serologic evaluation of VZV antibody • Biopsy with direct fluorescent examination using fluoresceinlabeled VZV antibody Differential Diagnosis • Primary herpes simplex/acute herpetic gingivostomatitis • Recurrent intraoral herpes simplex • Pemphigus vulgaris • Mucous membrane (cicatricial) pemphigoid .
Vesiculobullous Diseases 79 Treatment • Symptomatic management in primary infection • Antiviral drugs (especially acyclovir) in immunocompromised patients or patients with extensive disease • Systemic corticosteroids may be used to help control/prevent postherpetic neuralgia. • Pain control to prevent “CNS imprinting” Prognosis • Generally good • Recurrences more likely in immunosuppressed patients .
• Cervicofacial form is usually insidious in onset. and persistent swelling and discharge • Bone lesions may be destructive in nature. fungal. chronic enlargement of the jaw. actinomyces are anaerobic or microaerophilic Differential Diagnosis • Infection: nocardiosis. paresthesia. low-grade fever. extraoral abscess formation may be noted with drainage fluid containing yellow sulfur granules (bacterial colonies) Diagnosis • Sulfur granules (1–4 mm) in exudate • Peripheral club-like structures in bacterial colonies microscopically • Aerobic and anaerobic culture. chiefly the israelii species Clinical Presentation • Most common site is the mandible. • Presents typically as a hard. low-grade course. staphylococcal.80 PDQ ORAL DISEASE Ulcerative Conditions Actinomycosis Etiology • An infection caused by one of the Actinomyces group of bacteria. producing cervicofacial disease • Associated facial pain. with a longterm. with accompanying rarefaction and/or sclerosis or periostitis. streptococcal • Neoplasm (malignant) Treatment • Surgical débridement followed by prolonged antibiotic course (penicillin is drug of choice) • Surgical revision of extraoral drainage sites if indicated Prognosis • Excellent .
Ulcerative Conditions 81 .
pemphigus vulgaris. erosive/bullous lichen planus. and psychological stress. and malaise. • Ulcerated areas covered with grayish pseudomembrane • Often accompanied by dental plaque and calculus • Bleeding noted spontaneously or with minimal tissue manipulation • Extension of disease process into adjacent soft tissues noted on occasion Diagnosis • Observation of characteristic blunted. regional lymphadenitis. Clinical Presentation • Engorged. local hygiene.82 PDQ ORAL DISEASE Acute Necrotizing Ulcerative Gingivitis (Vincent’s Infection) Etiology • Fusobacterium nucleatum. Borrelia vincentii. intense smoking. nutritional deficiencies. fever. good oral hygiene. enlarged. and blunted interdental papillae with crateriform necrosis • Symptoms include pain. paraneoplastic pemphigus) Treatment • Local débridement. ultrasonic scaling. and home care . and other bacterial species including Prevotella and oral treponemes • Infection requires modification of local or systemic factors including immunosuppression. fetid breath. necrotizing interdental papillae with “punched-out” appearance • Lesions on gingiva only Differential Diagnosis • Leukemia • Immunosuppression-related conditions • Primary herpetic gingivostomatitis • Acute forms of leukemia • Vesiculobullous mucosal diseases (mucous membrane [cicatricial] pemphigoid.
• Identification and elimination of predisposing factor(s) • Underlying immunosuppression should be suspected if no improvement noted Prognosis • Excellent . metronidazole) may be beneficial.Ulcerative Conditions 83 • Rinses of chlorhexidine. topical povidone-iodine • Systemic antibiotics (tetracycline.
food allergy. zinc). major ulcers. Crohn’s disease.84 PDQ ORAL DISEASE Aphthous Stomatitis Etiology • Unknown—probably represents a focal immunodysfunction. • Human leukocyte antigen (HLA) subtype susceptibility a factor in some cases (-B12. trauma) • Alterations in barrier permeability may be a factor. -B51. dietary factors. and others) • Affects 18 to 27% of the population. Behçet’s disease. • Although likely immunologic in nature. as occur with human immunodeficiency virus/acquired immunodeficiency syndrome (HIV/AIDS). ulcerative colitis. increased stress/anxiety. herpetiform lesions • Minor variant (most common subtype) • Occasional • Single but more often multiple • Less than 1 cm in diameter • Oval to round shape • Healing within 7 to 14 days • Major variant (Sutton’s ulcers) • 1 cm or greater in diameter • Single or less commonly several • Deep • To ragged edges with elevated edematous margins . no viral or other infectious agent identified • Triggers vary from case to case (eg. gluten sensitivity. vitamin B12. hormonal changes. painful ulcers • Usually restricted to nonkeratinized oral and pharyngeal mucosa (not hard palate or attached gingiva) • Well-demarcated ulcers with yellow fibrinous base and erythematous halo • Three clinical forms: minor ulcers. prevalence is approximately 20% Clinical Presentation • Recurrent. folate. bone marrow suppression. the specific mechanism is undetermined. and dietary deficiencies (iron. neutropenia. self-limiting.
Diagnosis • Usually has diagnostic clinical appearance of focal. almost continuous ulcerations. should be addressed. • Systemic causative factors. • Tetracycline-based oral rinses may be helpful. usually minor or herpetiform) • In AIDS patients. a recurrent process • Positive family history Differential Diagnosis • Traumatic ulcer • Chancre • Recurrent intraoral herpes simplex stomatitis • Cyclic neutropenia Treatment • Symptomatic therapy may be adequate. if present. few lesions. or severe lesions) • Simple aphthosis (mild. disabling. episodic: 1– 4 episodes/yr. crops of 10 to 100 lesions • In nonkeratinized and keratinized tissues • Healing within 7 to 14 days • No etiologic role for herpes simplex virus • Recurrent aphthous stomatitis occurs as simple (minor) aphthosis (common) and complex (major) aphthosis (uncommon) • Complex aphthosis (severe. large. welldefined ulcers involving nonkeratinized mucosa • History helpful. lesions are typically more severe and may occur on any oral surface. • Corticosteroid therapy is the most rational approach and is a consistently effective treatment. or ointment 4 to 6 times/d to early lesions • Intralesional corticosteroid injections • Short-duration systemic corticosteroids (low to moderate doses) (continued) . • Topical corticosteroids as gels. creams.Ulcerative Conditions 85 • May persist for several weeks to months • Often heal with scarring • Herpetiform variant (least common variant) • Grouped superficial ulcers 1 to 2 mm in diameter.
topical tacrolimus.86 PDQ ORAL DISEASE • Other immunomodulating drugs may be helpful (dapsone. amelexanox). • Thalidomide treatment has shown efficacy in clinical trials. hydroxychloroquine. • Typically. • See “Therapeutics” section for details.2 mg/d) is sometimes beneficial. severity decreases as patient ages. • Colchicine (0. • Complex aphthosis • Needs medical evaluation for intercurrent disease • Chronic problem . Prognosis • Simple aphthosis • Excellent • Cannot be cured • Good control with corticosteroids is usually possible.6–1.
Ulcerative Conditions 87 .
with mucocutaneous presentation Clinical Presentation • Classic signs noted in the oral cavity. paralysis. usually secondary to vasculitis. inflammatory bowel disease) • Vascular thrombosis. meningoencephalitis) • Gastrointestinal problems (diarrhea. cutaneous problems) Differential Diagnosis • Erythema multiforme • Reiter’s syndrome . eye. and genitalia • Painful. sometimes debilitating. hematologic and other organ system manifestations Diagnosis • Oral aphthous ulcerations occurring at least three times per year in association with characteristic manifestations within other systems (ocular. and hypopyon • Cutaneous signs include the following: • Erythema nodosum–like lesions • Pustular folliculitis • Thrombophlebitis • Acneiform eruptions • Positive pathergy sign is characteristic: sterile pustule at site of sterile intradermal saline injection 48 hours prior • Other systems. iritis. oral and genital aphthous ulcers • Ocular lesions: painful conjunctivitis. retinitis. may be involved in the following manner: • Central nervous system (headache. uveitis. genital.88 PDQ ORAL DISEASE Behçet’s Disease Etiology • A multisystem disease secondary to an immunodysfunction associated with certain HLA subtypes • HLA-Bw51 clusters in those of Middle Eastern and Northern Asian descent • HLA-B12 noted more in those of European and North American descent.
Ulcerative Conditions 89 • Crohn’s disease • Mucous membrane (cicatricial) pemphigoid • Vulvovaginal-gingival variant of erosive lichen planus Treatment • Systemic corticosteroids • Immunosuppressive drugs (eg. cyclosporine. chlorambucil. methotrexate • Thalidomide has been proven helpful. TNFα inhibitors) • Azathioprine. interferon. Prognosis • Chronic • Manageable . • Dapsone and colchicine may be of value in some cases.
Diagnosis • Cytologic or histopathologic examination of tissue with identification of organism • Culture of sputum or fresh biopsy material • Potassium hydroxide preparation from lesion scraping Differential Diagnosis • Malignant tumor • Tuberculosis • Tertiary syphilis Treatment • Systemic antifungals: oral itraconazole Prognosis • Guarded • Untreated disease slowly progressive. productive cough • Chronic: granulomatous lesions of oropharyngeal mucosa. Mucocutaneous disease indicates disseminated disease. Mucosal lesions may mimic carcinoma. Paracoccidioides brasiliensis causes South American form and some endemic outbreaks in the United States. viscera. skin. bone. Extrapulmonary spread is hematogenous to skin. pulmonary signs mimicking tuberculosis • Skin and mucosal lesions are characterized by proliferative verrucous growth. night sweats. most infections are confined to the lungs. Clinical Presentation • Acute: pneumonitis. mucosa. ulceration. and the genitourinary tract. and scarring. meninges. weight loss. • Transmission is usually by spore inhalation. fatal .90 PDQ ORAL DISEASE Blastomycosis Etiology • Blastomyces dermatitidis produces the North American form of this disease. fever.
Ulcerative Conditions 91 .
epitheloid granulomas within submucosa Differential Diagnosis • Deep fungal diseases including blastomycosis • Mycobacterial infections • Tertiary syphilis and other treponemal infections • Major aphthous ulcers Treatment • Management of underlying intestinal symptoms (nonsteroid anti-inflammatory drugs. treatment as needed • Episodic burst of systemic corticosteroids in association with local management of oral lesions. diarrhea. • May present as orofacial granulomatosis such as granulomatous cheilitis • Lesions of pyostomatitis vegetans may be associated. oral mucosal lesions: monthly intralesional corticosteroid injections in areas of ulceration until improvement is noted. 7 to 10 days of prednisone with rapid taper to zero. Diagnosis • Correlation of mucosal lesions with intestinal symptoms of cramping. systemic corticosteroids) • Local. and associated weight loss • Oral mucosal biopsy results demonstrate noncaseating. with monitoring . if condition persists.92 PDQ ORAL DISEASE Crohn’s Disease Etiology • A granulomatous disease of unknown etiology • Genetic factors coupled with environmental influences appear of greatest importance Clinical Presentation • Extraintestinal/oral findings may include the following: • Nodular submucosal nodules of lips (granulomas) • Polypoid masses with fissures and ulceration along the buccal/labial sulcus • Oral ulcers of nonspecific/aphthous type may develop.
ileal-release budesonide Prognosis • Related to response of intestinal symptoms to treatment . 5-aminosalicylic acid.Ulcerative Conditions 93 • Management of any associated malabsorption may be helpful. • Metronidazole.
cryptococcosis.94 PDQ ORAL DISEASE Histoplasmosis Etiology • A fungal infection caused by Histoplasma capsulatum • Fungus endemic to Ohio and Mississippi River valleys • Transmission: spore inhalation • Oral lesions usually secondary to pulmonary lesions with hematogenous dissemination Clinical Presentation • General symptoms usually mild • Oral lesions associated with disseminated form/prior pulmonary lesions • Chronic ulcerations with necrosis. and blastomycosis) • Chronic traumatic ulcer • Tertiary syphilis Treatment • Sometimes none required • Amphotericin B • Ketoconazole. fluconazole. elevated nodular margins • May resemble squamous cell carcinoma • On the tongue. Diagnosis • Demonstration of organisms in biopsy specimen • Culture • Serologic demonstration of antigen or antibodies Differential Diagnosis • Tuberculosis • Squamous cell carcinoma • Other deep fungal infections (eg. • Oral ulcers persist until treatment of systemic disease. a cobblestone ulcer may be noted. itraconazole Prognosis • May recover spontaneously • Generally good unless immunosuppression present . coccidioidomycosis.
Ulcerative Conditions 95 .
and double-stranded deoxyribonucleic acid) Differential Diagnosis • Lichen planus • Candidiasis • Hypersensitivity/lichenoid eruption • Leukoplakia Treatment • Complex—dependent on LE variant present and level of disease expression • Systemic corticosteroids and immunosuppressive agents for SLE • Topical corticosteroid agents for intraoral lesions • Low-dose hydroxychloroquine • Intralesional corticosteroid injections . Diagnosis • Direct immunofluorescent examination of mucosal biopsy • Serologic correlation (antinuclear antibodies: anti–SS-A. keratotic.96 PDQ ORAL DISEASE Lupus Erythematosus Etiology • An autoimmune-/immunologically mediated condition • Antibodies demonstrable against an array of cytoplasmic and nuclear antigens • Most often occurs in women Clinical Presentation • Three forms are as follows: • Chronic cutaneous (CCLE) or discoid (DLE) • Subacute cutaneous (SCLE) • Systemic (SLE) • Black females have highest incidence • Predominates in women over 40 years • 80% of patients have concurrent cutaneous findings • 30 to 40% of SLE patients have oral mucosal findings • Oral mucosal lesions may appear lichenoid. and keratotic appearance • Oral findings are most common in CCLE or DLE. and erosive. erythematous. –SS-B. exfoliative. • Labial vermilion with crusted.
.Ulcerative Conditions 97 Prognosis • Good prognosis with CCLE or DLE form • Variable prognosis with SLE • SCLE has an intermediate prognosis between that of SLE and CCLE or DLE forms.
Absidia. Mucor genera • Noted chiefly in immunosuppressed individuals and in uncontrolled diabetics Clinical Presentation • Large. irregular. depending upon underlying systemic factors . necrotizing ulcers • Most often involves the palate with concomitant paranasal sinus involvement Radiographic Findings • Maxillary sinus opacification • Irregular sinus wall destruction Microscopic Findings • Tissue necrosis with fungal invasion into blood vessels • Nonseptate. broad hyphae Diagnosis • Radiographic findings • Microscopic findings Differential Diagnosis • Maxillary sinus neoplasia • Maxillary sinus aspergillosis • Soft tissue infarction • Soft tissue radionecrosis • Other deep fungal infections Treatment • Surgical débridement • Intravenous antifungal agents (amphotericin B. ketoconazole) • Control of underlying disease process Prognosis • Good. branching.98 PDQ ORAL DISEASE Mucormycosis (Zygomycosis) Etiology • Organisms of Zygomycetes class: Rhizopus.
Ulcerative Conditions 99 Photograph courtesy of Dr. . John Knapp.
often with minimal peripheral erythema • Ulcer base covered by fibrinous exudate • Wide variation in size of ulcers Diagnosis • Clinical appearance correlated with results of peripheral blood count Differential Diagnosis • Major aphthous ulcer • Traumatic ulcer • Necrotizing sialometaplasia • Squamous cell carcinoma Treatment • Identification and management of underlying neutropenia • Supportive therapy Prognosis • Relative to ability to manage underlying neutropenia .500/mm3 Clinical Presentation • Sharply defined ulcer(s).100 PDQ ORAL DISEASE Neutropenic Ulcer Etiology • Idiopathic or iatrogenic neutropenia • Usually noted when neutrophil count falls below 1.
Ulcerative Conditions 101 .
ulceration. atrophy. contiguous ulcers form. and pseudomembrane formation • Generalized pain and dysfunction • Ultimately. antibacterial therapy • Topical agents • Water-soluble polymer films • Antimicrobials • Saline rinses • Antifungal agents • Granulocyte-macrophage colony-stimulating factor • Local and hygiene measures Prognosis • Good • Improves slowly subsequent to treatment . • Usually begins within 7 to 10 days following the start of treatment • Exacerbated by radiation-induced xerostomia or chemotherapy/ cytoreductive therapy Diagnosis • History and appearance Differential Diagnosis • Erythema multiforme • Chemotherapy-induced stomatotoxicity • Acute erythematous candidiasis • Neutropenic ulcer Treatment • Systemic antiviral.102 PDQ ORAL DISEASE Radiation-Induced Mucositis Etiology • Local tumoricidal doses of ionizing radiation • Destruction of germinative layers of oral mucosal epithelium within radiation portal • May be enhanced by intraoral gram-negative bacteria Clinical Presentation • Mucosal erythema. broadly based. necrosis.
Ulcerative Conditions 103 .
cords of epithelial cells • Individual cells with nuclear pleomorphism. induration. ill-defined margins in later stages Microscopic Findings • Usually well differentiated to moderately differentiated • Invasive islands. cervical lymph node metastases Radiographic Findings • May erode or invade adjacent bone in later stages • Irregular. usually a white or red-white focal surface alteration • Later stages with ulceration. dyskeratosis • Architectural disorganization of proliferating cells Diagnosis • Microscopic analysis of tissue specimen (biopsy) Differential Diagnosis • Chronic traumatic ulcer • Primary syphilis • Deep fungal infection • Palatal necrotizing sialometaplasia • Keratoacanthoma (labial) . destructive. floor of mouth • Lower lip vermilion surface also a common location • Advanced-stage disease has associated limitation of movement.104 PDQ ORAL DISEASE Squamous Cell Carcinoma Etiology • Majority (approximately 80%) related to tobacco and alcohol abuse • Some cases may be virus associated (human papillomavirus types 16 and 18) • Stepwise progression of genetic alterations now defined from normal to dysplasia to carcinoma Clinical Presentation • Early. increased nuclearto-cytoplasmic ratio. trismus. elevated margins • Most common sites: lateral tongue.
• Combined surgery and radiation therapy for more advancedstage lesions • Adjuvant chemotherapy plays a role in advanced disease. Prognosis • Results are stage related as follows: • Stages 1 and 2: generally good prognosis • Stages 3 and 4: generally fair to poor prognosis .Ulcerative Conditions 105 Treatment • Surgical excision is the treatment of choice.
midline of tongue. leukoplakia features • Gumma: destructive. especially • Congenital form • Hutchinson’s triad including mulberry molars. secondary.106 PDQ ORAL DISEASE Syphilis Etiology • Treponema pallidum spirochete Clinical Presentation • Four clinical types (primary. palate. painless. appearance • Direct smear in primary.and secondary-stage lesions (dark field) . painless • Intraoral chancre is an ulcer covered by a pseudomembrane • Lesion is highly infectious • Regional cervical lymphadenopathy • Spontaneous resolution • Secondary stage • Evolves after 6 weeks to 6 months if patient is untreated • Reddish brown macular rash periorally. indurated. solitary granulomatous ulcer. congenital form) plus neonatal form • Primary stage (oral) • Initial sign usually a firm nodule/papule • Labial ulceration most common presentation • Ulcer firm. or erosions • Mucous patches orally (ulcers covered by mucoid exudate) • Lymphadenopathy • Highly infectious • Spontaneous resolution • Tertiary stage • Develops over 3 to 10 years after primary infection if untreated or inadequately treated (more rapidly in immunocompromised patients) • Glossitis: atrophic. irregular lesions. barrel-shaped incisors Diagnosis • Clinical history. generalized cutaneous rash • Oral lesions are split papule at lip commissures. serpiginous ulcers. and tertiary stages.
VDRL [Venereal Disease Research Laboratories] test): positivity noted in last phase of primary stage • Biopsy Differential Diagnosis • Deep fungal infection • Traumatic ulcer • Squamous cell carcinoma • Leukoplakia • Midline granuloma/Wegener’s granulomatosis Treatment • Antibiotics • Parenteral penicillin (penicillin G benzathine) or ceftriaxone • Oral tetracycline or doxycycline Prognosis • Excellent in primary and secondary stages • Fair in late (tertiary) phase .Ulcerative Conditions 107 • Serologic studies (eg.
endothelial proliferation • Inflammatory infiltrate with prominent macrophages • Underlying muscle injury present with eosinophilic infiltrate Diagnosis • History and appearance • Biopsy results/microscopic findings Differential Diagnosis: Clinical • Squamous cell carcinoma • Major aphthous ulcer • Lymphoma • Syphilis • Granulomatous disease • Sarcoidosis • Wegener’s granulomatosis • Tuberculosis Differential Diagnosis: Microscopic • Lymphoma • Angiolymphoid hyperplasia with stromal eosinophilia .108 PDQ ORAL DISEASE Traumatic Granuloma (Traumatic Eosinophilic Ulcer) Etiology • A benign. crateriform ulcer • Several weeks mean duration • 60% occur on the tongue (lateral/ventral) • Average diameter 1 to 2 cm Microscopic Findings • Crateriform ulcer with fibrinous surface • Deeper areas with granulation tissue. self-limiting. reactive process of oral mucosa of unknown origin • Some cases with no history of antecedent trauma Clinical Presentation • Rapid onset • Painful. indurated.
. • Rare cases have multiple recurrences.Ulcerative Conditions 109 Treatment • Excision • Observation only • Topical or intralesional corticosteroids Prognosis • Healing usually within 10 days if excised • Most lesions heal after a few to several weeks without recurrence.
110 PDQ ORAL DISEASE Traumatic Ulcer Etiology • Accidental/functional or factitious injury Clinical Presentation • Tender to very painful • Ulcer with yellow. fibrinous center and well-defined margins • Inflammatory/erythematous periphery Microscopic Findings • Fibrinous surface • Mixed inflammatory infiltrate • Granulation tissue at base of lesion Diagnosis • History of trauma • Evaluation for ill-fitting dental prosthesis or orthodontic appliance • Nonspecific histologic findings Differential Diagnosis • Aphthous ulcer • Neutropenia-related ulcer • Factitial ulcer • Squamous cell carcinoma • Primary syphilis (chancre) Treatment • None except elimination of cause • Healing within 10 days Prognosis • Excellent .
Ulcerative Conditions 111 .
streptomycin. less commonly M. Microscopic Findings • Centrally necrotic granulomas with peripheral multinucleated Langhans’ giant cells • Positive Fite or Ziehl-Neelsen tissue staining of microorganisms Diagnosis • Clinical appearance and lesion persistence • Histopathology • Tuberculin skin test. . aviumintracellulare • Oral lesions form in relation to extension of disease beyond the pulmonary focus • Increased incidence in immunocompromised patients Clinical Presentation • Chronic. two-step Mantoux test • Culture Differential Diagnosis • Squamous cell carcinoma • Syphilis • Deep mycotic infection • Traumatic eosinophilic ulcer • Lymphoma Treatment • Systemic chemotherapy: isoniazid. prognosis is fair. rifampin. and others • Note: Multidrug-resistant organism may be present. Prognosis • Good • In the immunosuppressed patient.112 PDQ ORAL DISEASE Tuberculosis Etiology • Mycobacterium tuberculosis usually. • Intrabony lesions are lytic and sequestrate with radiographic features of osteomyelitis. nonhealing ulcer with induration • Borders may be raised or rolled.
Ulcerative Conditions 113 .
necrosis. including midline granuloma • Late-stage syphilis • Deep fungal infection • Tuberculosis • Major aphthous ulcers .114 PDQ ORAL DISEASE Wegener’s Granulomatosis Etiology • Unknown • A necrotizing vasculitis with preferential involvement of the respiratory tract early in its course • Oral involvement unusual and characterized by ulceration and tissue destruction Clinical Presentation • Jaw pain. normocytic. • Classic triad of upper airway. lung. • Tissue biopsy for microscopic features • Laboratory studies show the following: • Antineutrophil cytoplasmic antibodies (ANCAs)—two staining patterns: cytoplasmic ANCA (high specificity) and perinuclear ANCA • Mild. normochromic anemia (in 50%) • Elevated erythrocyte sedimentation rate Differential Diagnosis • Lymphoma. and kidney involvement not required for diagnosis • May remain localized for prolonged periods prior to multiorgan involvement Microscopic Findings • Vasculitis. gingival inflammation with petechiae or hyperplasia. and granulomatous inflammation Diagnosis • Oral or upper airway biopsy is helpful in less than one-half of cases. palatal ulceration with possible perforation • Painful salivary gland enlargement may be encountered.
Ulcerative Conditions 115 Treatment • Cyclophosphamide/prednisone • Trimethoprim/sulfamethoxazole (as monotherapy or in combination with immunosuppressive therapy) Prognosis • Fair • Secondary complications related to long-term immunosuppression .
vomiting.116 PDQ ORAL DISEASE Pigmentary Disorders Addison’s Disease Etiology • Adrenal cortical atrophy—85% idiopathic (?autoimmune) • Oral manifestations due to secondary melanocyte stimulation by increased levels of adrenocorticotropic hormone (ACTH) or β-lipotropin Clinical Presentation • Brown macular pigmentation of local or diffuse quality • Pigmentation usually seen in association with cutaneous bronzing. hypotension Diagnosis • Confirmation of hypoadrenocorticism by plasma ACTH levels after challenge/stimulation • Biopsy of mucosa shows melanosis Differential Diagnosis • Smoker’s melanosis • Physiologic/ethnic pigmentation • Heavy metal deposition/argyrosis • Medication-related pigmentation • Peutz-Jeghers syndrome Treatment • Management of underlying adrenal insufficiency by corticosteroid replacement therapy Prognosis • Good with replacement therapy . weight loss. nausea. salt craving. weakness.
Pigmentary Disorders 117 .
usually well defined. buccal mucosa • Occasionally may be visible radiographically Diagnosis • Radiographs may be useful (intraoral film placement) • Biopsy may be necessary if clinical diagnosis is in doubt or to rule out lesions of melanocytic origin Differential Diagnosis • Vascular malformation • Mucosal nevus • Melanoma • Mucosal melanotic macule • Melanoacanthoma Treatment • Biopsy or observation only Prognosis • Little clinical significance if untreated . alveolar mucosa. but may be diffuse with no associated signs of inflammation • Typically in attached gingiva.118 PDQ ORAL DISEASE Amalgam Tattoo Etiology • Implantation or passive/frictional transfer of dental silver amalgam into mucosa Clinical Presentation • Gray to black focal macules.
Pigmentary Disorders 119 .
120 PDQ ORAL DISEASE Melanoacanthoma Etiology • A reactive and reversible alteration of oral mucosal melanocytes and keratinocytes • Usually associated with local trauma Clinical Presentation • Unilateral dark plaque. rarely multiple. bilateral • Most often noted among Blacks and other non-Caucasians • Occurs more often in women than men by a ratio of 3:1 • History of trauma and local irritation • Forms rapidly. most often on buccal/labial mucosa • Asymptomatic melanotic pigmentation Diagnosis • Clinical history of rapid onset • Histologic evaluation • Scattered dendritic melanocytes within spongiotic and acanthotic epithelium • Increased number of melanocytes along basal layer as single units Differential Diagnosis • Melanoma • Drug-induced pigmentation • Smoker’s melanosis • Mucosal melanotic macule • Mucosal nevus • Amalgam tattoo Treatment • None after establishing the diagnosis • Often resolves spontaneously Prognosis • Excellent .
Pigmentary Disorders 121 .
• Usually arises on maxillary gingiva and hard palate • May exhibit early in situ phase: a macular. as in skin. • Amelanotic forms may require use of immunohistochemical identification: S-100 protein. occasionally with intraepithelial spread • Later infiltration into lamina propria and muscle • Strict correlation to cutaneous malignant melanoma is not well established. HMB-45. a similar horizontal or in situ growth phase often precedes the vertical invasive phase. usually pigmented mass Microscopic Findings • Early stage: atypical melanocytes at epithelial–connective tissue interface. Melan-A expression Diagnosis • Biopsy • High index of suspicion Differential Diagnosis • Mucosal nevus • Extrinsic pigmentation • Melanoacanthoma • Kaposi’s sarcoma • Vascular malformation • Amalgam tattoo • Mucosal melanotic macule . although. pigmented patch with irregular borders • Progression to deeply pigmented.122 PDQ ORAL DISEASE Mucosal Malignant Melanoma Etiology • Unknown • Cutaneous malignant melanoma with relation to sun exposure or familial-dysplastic melanocytic lesions Clinical Presentation • Rare in oral cavity (< 1% of all melanomas) and sinonasal tract • Most cases occur in those older than 30 years of age. nodular quality with ulceration • May arise de novo as a pigmented or amelanotic nodule • Rarely may be metastatic to the oral cavity as a nodular.
25 mm) Prognosis • Generally poor for most oral malignant melanomas • Less than 20% survival at 5 years in most studies . resection (including maxillectomy) for large. deeper lesions • Neck dissection in cases of deep invasion (< 1.Pigmentary Disorders 123 Treatment • Surgical excision • Marginal parameters related to depth of invasion and presence of lateral growth • Wide surgical margins.
some drug-induced • Multiple lesions suggest syndrome association. as follows: • Peutz-Jeghers syndrome • Laugier-Hunziker phenomenon • Carney’s syndrome • LEOPARD syndrome Clinical Presentation • Most in adulthood (fourth decade and beyond) • Most are solitary and well circumscribed • Lower lip vermilion border most common site. Laugier-Hunziker) . some postinflammatory.124 PDQ ORAL DISEASE Mucosal Melanotic Macule and Ephelides Etiology • Most idiopathic. LEOPARD. uniformly pigmented. mostly in young women (labial melanotic macule) • Buccal mucosa. and attached gingiva also involved (mucosal melanotic macule) • Usually brown. Peutz-Jeghers. round to ovoid shape with slightly irregular border • Usually < 5 mm in diameter Microscopic Findings • Normal melanocyte density and morphology • Increased melanin in basal cells and subjacent macrophages (mucosal melanotic macule) • Increased melanin in basal cells with elongated rete pegs (ephelides) Diagnosis • Biopsy Differential Diagnosis • Melanoacanthoma • Mucosal melanotic macule • Congenital syndromes (Carney’s. palate.
particularly if on palate or alveolar mucosa. macule should be removed to rule out malignant melanoma.Pigmentary Disorders 125 Treatment • Observation • Biopsy for esthetics • If increase in size or development of atypical signs occurs. Prognosis • Excellent .
phenolphthalein. minocycline. in situ melanoma must be ruled out by biopsy. mucosal melanotic macule. Treatment • Investigation of cause and elimination if possible Prognosis • Excellent . also nonmetal agents. a typical gray to black color is seen along the gingival margin or areas of inflammation. cis-platinum. purpura. • Darkened alveolar bone with minocycline therapy (10% at 1 year. or ingestion of.126 PDQ ORAL DISEASE Mucosal Pigmentation: Extrinsic (Drug or Metal Induced) Etiology • Occupational exposure—metals vapors (lead. 20% at 4 years of therapy) Diagnosis • History of exposure to. heavy metals or drugs • Differentiation from melanocyte-related pigmentation by biopsy if necessary Differential Diagnosis • When localized: amalgam tattoo. ecchymosis • When generalized: ethnic pigmentation. clofazimine. • Palatal changes characteristic with antimalarial drugs and minocycline • Most medications cause color alteration of buccal-labial mucosa and attached gingiva. mucosal nevus. silver. and others Clinical Presentation • Focal to diffuse areas of pigmentary change • If heavy metals are the cause. mercury) • Therapeutic—metal salt deposits (bismuth. zidovudine. chlorpromazine. Kaposi’s sarcoma. melanoacanthoma. ephelides. gold). such as chloroquine. malignant melanoma. Addison’s disease • If asymmetric.
Pigmentary Disorders 127 .
128 PDQ ORAL DISEASE Nevus Etiology • Unknown • Lesion of melanocytic origin within mucosa and skin Clinical Presentation • Usually elevated. junctional and compound nevi (no dysplastic nevi occur orally) • Nevus cells are oval/round and are found in unencapsulated nests (theques). • Other variants are rare. symmetric papule • Pigmentation usually uniformly distributed • Common on skin. • Melanin production is variable. unusual intraorally • Palate and gingiva most often involved Microscopic Findings • Most are intramucosal (“dermal”) • Blue nevi are deeply situated and are composed of spindled nevus cells. Diagnosis • Clinical features • Biopsy Differential Diagnosis • Melanoma • Varix • Amalgam tattoo/foreign body • Mucosal melanotic macule • Kaposi’s sarcoma • Ecchymosis • Melanoacanthoma Treatment • Excision of all pigmented oral lesions to rule out malignant melanoma is advised. Prognosis • Excellent . • Malignant transformation of oral nevi probably does not occur.
Pigmentary Disorders 129 .
Microscopic Findings • Diffuse unencapsulated proliferation of spindle-shaped melanocytes within dermis/submucosa. parallel to surface • Pigment production may be florid.130 PDQ ORAL DISEASE Nevus of Ota Etiology • Idiopathic/congenital • A proliferation of dermal melanocytes over a specific anatomic distribution Clinical Presentation • Macular. grayish blue discoloration of skin and mucosa over the distribution of the ophthalmic and maxillary branches of the trigeminal nerve • Unilateral distribution • Sclera on the involved side may be affected. Diagnosis • Clinical presentation Treatment • None • Cosmetic Prognosis • Excellent .
Pigmentary Disorders 131 .
old-time antimalarials • Antibiotics: tetracycline group. Some are related to the deposition of a drug complex or a metabolized drug. Diagnosis • History • Clinical appearance Differential Diagnosis • Physiologic changes • Smoker’s melanosis • Mucosal melanotic macule Treatment • Drug withdrawal Prognosis • Good Drugs Capable of Producing Tissue Pigmentation • Antimalarials: chloroquine.132 PDQ ORAL DISEASE Pigmentation Disorders: Drug Induced Etiology • Therapeutic drug-related tissue pigmentation • Many drugs may cause change—see listing below Clinical Presentation • Macular mucosal discoloration (brown. mepacrine. black) • Palate and gingiva are most common sites affected • In addition to mucosal changes. minocycline • Antivirals: azidothymidine • Phenothiazine: chlorpromazine . quinidine. Microscopic Findings • Most cases are due to increased melanin production. teeth in adults and children may be bluish gray owing to minocycline/tetracycline use (see “Tetracycline Staining” on page 138). gray.
lead Hormones: ACTH. cyclophosphamide. silver nitrate. cis-platinum • Other: methyldopa .Pigmentary Disorders 133 • • • • Clofazimine Heavy metals: gold. bismuth. oral contraceptives Cancer/chemotherapy drugs: busulfan. mercury salts.
134 PDQ ORAL DISEASE Pigmentation Disorders: Physiologic Etiology • Normal melanocyte activity Clinical Presentation • Seen in all ages • Symmetric distribution over many sites. gingiva most commonly • Surface architecture. texture unchanged Diagnosis • History • Distribution Differential Diagnosis • Mucosal melanotic macule • Smoking-associated melanosis • Superficial malignant melanoma Treatment • None Prognosis • Excellent .
Pigmentary Disorders 135 .
mepacrine. especially females taking birth control pills or hormone replacement • Melanocytes stimulated by a component in tobacco smoke Clinical Presentation • Brownish discoloration of alveolar and attached labial gingiva. • Degree of pigmentation is positively influenced by female hormones (birth control pills. symmetric gingival pigmentation occurs most often. heavy smoking • Biopsy • Clinical appearance Differential Diagnosis • Physiologic pigmentation • Addison’s disease • Medication-related pigmentation (drug-induced pigmentation by chloroquine. if smoking is discontinued Prognosis • Good. clofazimine. with smoking cessation . quinidine.136 PDQ ORAL DISEASE Pigmentation Disorders: Smoker’s Melanosis Etiology • Melanin pigmentation of oral mucosa in heavy smokers • May occur in up to 1 of 5 smokers. buccal mucosa • Pigmentation is diffuse and uniformly distributed. or zidovudine) • Malignant melanoma Treatment • None • Reversible. chlorpromazine. hormone replacement therapy). Microscopic Findings • Increased melanin in basal cell layer • Increased melanin production by normal numbers of melanocytes • Melanin incontinence Diagnosis • History of chronic.
Pigmentary Disorders 137 .
tetracycline ingestion causes staining after tooth formation is complete: reparative (secondary) dentin cementum may be stained. Differential Diagnosis • Dentinogenesis imperfecta Treatment • Restorative/cosmetic dental techniques Prognosis • Good . Clinical Presentation • Yellowish to gray (oxidized tetracycline) color of enamel and dentin • May be generalized or horizontally banded depending on duration of tetracycline exposure • Alveolar bone may also be stained bluish red (particularly with minocyline use.138 PDQ ORAL DISEASE Tetracycline Staining Etiology • Prolonged ingestion of tetracycline or its congeners during tooth development • Less commonly. 10% after 1 year and 20% after 4 years of therapy). Diagnosis • Clinical appearance and history • Fluorescence of teeth may be noted with ultraviolet illumination.
Pigmentary Disorders 139 .
11. exophytic papillary growths with pedunculated outline • May be solitary or multiple and variably sized. 16. lingual frenum) • Pink to whitish pink.140 PDQ ORAL DISEASE Verrucal-Papillary Lesions Condyloma Acuminatum Etiology • A sexually transmitted disease • Associated with human papillomavirus (HPV) types 6. up to 2 to 3 cm • Can present as papillomatosis of upper respiratory tract Diagnosis • Location and appearance • Demonstration of koilocytotic cellular changes on biopsy • In situ hybridization or polymerase chain reaction reveals specific HPV subtype • Electron microscopy demonstrates intranuclear virions Differential Diagnosis • Focal epithelial hyperplasia • Multiple intraoral verruca vulgaris • Squamous papilloma Treatment • Conservative removal • Conventional surgery • Laser ablation • Topical podophyllin . and 18 most often • Can result in autoinoculation of other sites via trauma • Lesions located at the site of contact/traumatic event Clinical Presentation • Usually on nonkeratinized tissues in immunocompetent patients (soft palate.
Verrucal-Papillary Lesions 141 Prognosis • Recurrences common • Contagiousness and autoinoculation are considerations. .
142 PDQ ORAL DISEASE Focal Epithelial Hyperplasia Etiology • A viral infection (HPV 13 or 32). probably secondary through horizontal viral transmission • Often occurs in native Americans Clinical Presentation • Numerous. usually found in childhood • Familial/ethnic clustering often noted. anastomosing epithelial ridges with occasional superficial koilocytotic changes Diagnosis • Multiple. slightly raised whitish pink asymptomatic papules and irregular plaques that may become confluent • Size of lesions ranges from a few millimeters to coalescent papules several centimeters in dimension Microscopic Findings • Well-defined acanthotic features • Broadened. lesions usually regress spontaneously • Excision if esthetic needs demand • Intralesional interferon therapy Prognosis • Excellent • No reported malignant transformation . characteristic lesions • Biopsy findings • In situ deoxyribonucleic acid hybridization to demonstrate HPV subtype • Ultrastructural localization of intranuclear virions Differential Diagnosis • Condyloma acuminatum • Multiple verruca vulgaris Treatment • None.
Verrucal-Papillary Lesions 143 .
24. may be related to several factors. firm nodule • Central keratin core • Occasionally regresses spontaneously • Extremely rare intraorally Diagnosis • Clinical evaluation. peripheral epidermis and mature. as follows: • Viral—HPV subtypes 11. no invasion below adnexa. including lip • Initially erythematous papule • Rapid growth over 4 to 8 weeks • Nodular. 33. follow-up • Histopathology shows keratin plus normal.144 PDQ ORAL DISEASE Keratoacanthoma Etiology • Unknown. 57 • Altered expression of cell cycle proteins including cyclin E. premature keratinization. hemispheric. p53. 13. PCNA • Keratinocyte dedifferentiation reflected in deficient desmoglein production • Immunosuppression • Sun damage • May represent a highly differentiated form of squamous cell carcinoma • May indicate underlying alimentary neoplasia (Muir-Torre syndrome) Clinical Presentation • Usually solitary on sun-exposed areas. marked pseudoepitheliomatous hyperplasia Differential Diagnosis • Squamous cell carcinoma • Molluscum contagiosum • Warty dyskeratoma • Verruca vulgaris • Pilomatricoma • Condyloma acuminatum • Squamous papilloma .
Verrucal-Papillary Lesions 145 Treatment • Observation and careful follow-up • Local excision • Cryotherapy • Intralesional chemotherapy (methotrexate. or bleomycin) Prognosis • Excellent . 5-fluorouracil.
• Often combined with blood vessels • Rare variant may occur bilaterally on mandibular alveolar ridge of neonates Diagnosis • Biopsy • Lymphangiography Differential Diagnosis • Neurofibroma (deep) • Hemihypertrophy syndromes Treatment • Excision • If large lesions are stable. • Deeper lesions present as painless fluctuant masses such as macroglossia. observation • Sclerotherapy Prognosis • Variable. depending upon depth and extent of lesion • Cavernous variant has guarded prognosis . buccal mucosa. palate • Facial asymmetry may be a presenting sign.146 PDQ ORAL DISEASE Lymphangioma Etiology • A benign proliferation of lymphatic vasculature • Usually congenital in nature Clinical Presentation • Superficial or deep in location • Typically waxes and wanes in size • Most commonly involves the tongue followed by lips. • Superficial mucosal lymphangiomas resemble caviar or frog’s eggs.
Verrucal-Papillary Lesions 147 .
may note pseudoepitheliomatous hyperplasia Differential Diagnosis • Contact stomatitis • Chronic candidiasis • Denture stomatitis Treatment • Establishment of good oral hygiene • Possible antifungal therapy • Surgical removal of affected mucosa. if excessive tissue hyperplasia • Relining/remaking of denture Prognosis • Excellent .148 PDQ ORAL DISEASE Papillary Hyperplasia (Palatal Papillomatosis) Etiology • Generally attributed to ill-fitting maxillary denture • Often associated with 24 h/d denture wearing • Candida albicans overgrowth common • May be noted in habitual mouth breathers (nondenture wearers) Clinical Presentation • Erythematous palatal vault beneath denture • Nodular papillary excrescences • Generally asymptomatic Diagnosis • Clinical appearance • Biopsy results show fibrous and epithelial papillary hyperplasia.
Verrucal-Papillary Lesions 149 .
• Folds of nodular to hyperplastic tissue (“cobblestoning”) Microscopic Findings • Neutrophilic and eosinophilic infiltrate into epithelium producing microabscesses • Infiltration between epithelial clefts • Epithelial hyperplasia Diagnosis • Correlation with underlying gastrointestinal disease. Clinical Presentation • Mucosal pustules. such as the following: • Ulcerative colitis • Crohn’s disease • Sclerosing cholangitis • Malabsorption syndrome Differential Diagnosis • Oral Crohn’s disease • Pseudomembranous (acute) candidiasis • Melkersson-Rosenthal syndrome • Orofacial granulomatosis • Acanthosis nigricans Treatment • Successful management of underlying gastrointestinal disease • Local anti-inflammatory agents • Dapsone or sulfapyridine systemically .150 PDQ ORAL DISEASE Pyostomatitis Vegetans Etiology • A pustular eruption usually associated with inflammatory bowel disease and skin disease • Liver dysfunction (sclerosing cholangitis) may be associated in some cases. edema • Erosions and ulcers may form with serpiginous outlines (“snail tracks”). erythema.
Verrucal-Papillary Lesions 151 Prognosis • Correlates with that of systemic disease .
gingiva. tongue. Clinical Presentation • Exophytic. buccal mucosa may also be involved Microscopic Findings • Epithelial hyperplasia with fibrovascular cores • Papillary projections may be sharp to blunt. • Epithelium may be dysplastic in some lesions from human immunodeficiency virus–positive patients.152 PDQ ORAL DISEASE Squamous Papilloma Etiology • A benign epithelial proliferation • HPV is found in most cases. papillary mass. several subtypes have been identified. measuring less than 1 cm • Usually pedunculated and soft in texture • White • Usually solitary. Diagnosis • Clinical appearance • Biopsy features Differential Diagnosis • Condyloma acuminatum • Verruca vulgaris • Focal epithelial hyperplasia • Verrucous carcinoma Treatment • Surgical excision Prognosis • Low recurrence rate . especially HPV 6 and 11. may be multiple • Favors soft palate. uvula.
Verrucal-Papillary Lesions 153 .
or 11 Clinical Presentation • Papular to nodular and exophytic appearance • Surface texture is cauliflower-like or verruciform in nature • Perioral skin lesions may be brownish. • May be pedunculated or broad based • Intraoral sites of predilection include the lips. and attached gingiva. • Oral mucosal lesions are usually white to pink. palate. 6. • Multiple oral lesions may be evident in immunocompromised patients.154 PDQ ORAL DISEASE Verruca Vulgaris (Oral Warts) Etiology • Infection of mucosal epithelium by members of the human papillomavirus group—usually HPV 2. 4. Diagnosis • Clinical appearance • Microscopic findings • Immunohistochemical demonstration of HPV common antigen Differential Diagnosis • Focal epithelial hyperplasia • Keratoacanthoma • Papillary squamous carcinoma • Squamous papilloma • Condyloma acuminatum . Microscopic Findings • Surface hyperkeratosis • Granulosis • Koilocytosis • Acquired immunodeficiency syndrome–associated oral warts may appear dysplastic microscopically.
Verrucal-Papillary Lesions 155 Treatment • Excision • Laser surgery • Cryosurgery • Electrosurgery Prognosis • Excellent in immunocompetent host • Recurrence not uncommon .
especially smokeless tobacco • A primary or ancillary role for HPV is suspected. irregular. • Early. and indurated. • May be preceded by keratotic patch (see “Verrucous Hyperplasia” on page 158) Clinical Presentation • One-half of cases involve the buccal mucosa. lesions become exophytic. • Metastases are rare. . superficial lesions often are interpreted as verrucous hyperplasia. • Attached gingiva is involved in one-third of cases. exophytic and endophytic squamous cell carcinoma often associated with tobacco use. • Advancing lesions push into adjacent tissues. blunt masses of epithelium extending into submucosa • Intense lymphocytic infiltrate adjacent to invasive front Diagnosis • Microscopic findings • Full-thickness specimen is necessary to establish diagnosis Differential Diagnosis • Verrucous hyperplasia • Papillary squamous cell carcinoma • Proliferative verrucous leukoplakia Treatment • Wide excision • Radiation therapy may be effective. • Dedifferentiation may occur spontaneously or after radiation therapy.156 PDQ ORAL DISEASE Verrucous Carcinoma Etiology • A well-differentiated. • Late lesions invade the periosteum and destroy bone. Microscopic Findings • Well-differentiated.
.Verrucal-Papillary Lesions 157 Prognosis • Excellent • Local recurrence is a distinct possibility.
158 PDQ ORAL DISEASE Verrucous Hyperplasia Etiology • Unknown. bosselated epithelial ridges • Well-differentiated cellular features • Some similarity to early verrucous carcinoma Diagnosis • Microscopic features Differential Diagnosis • Verrucous carcinoma • Papillary squamous cell carcinoma • Proliferative verrucous leukoplakia Treatment • Excision or ablation (eg. tobacco (smokeless) associated most commonly • Role of HPV is unclear. electrocautery) • Continued observation Prognosis • Good with complete excision • Recurrence is common. keratotic fronds of epithelium • May be part of the proliferative verrucous leukoplakia spectrum Microscopic Findings • Papillary to verruciform surface projections • Keratin varies in thickness • Broad. papillary. • A possible precursor to verrucous carcinoma Clinical Presentation • Exophytic. . laser.
Verrucal-Papillary Lesions 159 .
or tenderness • Radiopacity with peripheral radiolucent halo • Mass fused to root of affected tooth Radiographic Findings • Focal radioactivity • Obscuration of root apex • Thin radiolucent rim Diagnosis • Radiographic findings • History of pain/tenderness • Histologically: abundant number of cementoblasts are associated with an irregular network of hard tissue (cementum) • Microscopically similar to osteoid osteoma Differential Diagnosis • Focal osseous dysplasia • Ossifying fibroma • Osteoma Treatment • Enucleation (with associated tooth) Prognosis • Excellent .160 PDQ ORAL DISEASE Connective Tissue Lesions Cementoblastoma Etiology • An uncommon. benign tumor of mesenchymal odontogenic origin • Unknown stimulus Clinical Presentation • Usually affects patients under the age of 30 years • Mandibular molar-premolar region is most common site • Jaw expansion. pain.
Connective Tissue Lesions 161 .
atopic. may be familial in some cases • Alternative etiologies include infectious. • Biopsy results may show labial salivary gland hyperplasia and ductal ectasia. actinic. and factitious origins Clinical Presentation • Usually involves lower lip of adult males (may occasionally involve both lips) • Tender eversion and enlargement of lip • Mucoid to purulent secretion at minor salivary gland orifices Diagnosis • Microscopy shows nonspecific inflammation.162 PDQ ORAL DISEASE Cheilitis Glandularis Etiology • Unknown. • Sialadenitis Differential Diagnosis • Granulomatous cheilitis (orofacial granulomatosis) • Atopic cheilitis • Actinic or photosensitivity cheilitis Treatment • Surgical excision • Suppressive therapy with broad-spectrum antibiotics • Intralesional corticosteroid injections Prognosis • Chronic • Good .
Connective Tissue Lesions 163 .
PDQ ORAL DISEASE
Etiology • Chronic low-grade trauma/irritation • A reactive (hyperplastic), rather than neoplastic, process Clinical Presentation • Firm • Same as or more pale than surrounding tissue • Pedunculated or broadly based (sessile) fibrous mass with a smooth, elevated surface • Asymptomatic and slow growing • May be secondarily ulcerated or keratotic • Typically in regions accessible to trauma: buccal mucosa, lateral tongue margin, lower lip Diagnosis • Appearance • Location Differential Diagnosis • Other submucosa/connective soft tissue tumors, as follow: • Granular cell tumor • Neurofibroma • Lipoma • Schwannoma • Salivary tumor • Metastatic tumor Treatment • Conservative local excision Prognosis • Excellent
Connective Tissue Lesions
PDQ ORAL DISEASE
Etiology • Unknown • A dysplastic process or developmental lesion of bone Clinical Presentation • An asymptomatic tumor-like mass or deformity of bones • May be monostotic (80%) or polyostotic (20%) • Uncommonly, the polyostotic form may occur with endocrine hyperfunction and focal cutaneous pigmentation (McCuneAlbright syndrome). • Slow-growing, painless swelling of affected bone(s) • Mandibular body most common site • Facial asymmetry a frequent presenting sign • Tooth displacement and malocclusion common • Maxillary jaw lesions may be accompanied by involvement of the zygoma, sphenoid, and, less commonly, the occiput (the craniofacial variant). Radiographic Findings • Ill-defined, uniformly radiopaque enlargement with “groundglass” qualities and diffuse, blended margins • Mandibular lesions may show loculation. • The craniofacial form may show skull base thickening. • Intraoral films may show lamina dura obscurity. Diagnosis • Clinical appearance • Radiographic qualities • Biopsy showing typical irregular trabeculae of woven bone (“Chinese characters”) and fibroblastic, vascularized stroma Differential Diagnosis • Chronic sclerosing osteomyelitis • Localized Paget’s disease • Osteosarcoma • Cemento-osseous dysplasias
Connective Tissue Lesions
Treatment • Cosmetic recontouring, if necessary • Observation only, if lesions are minimally developed and stable Prognosis • Most stabilize in adult life • Some relapse noted in up to one-half of surgically recontoured cases • Malignant transformation rare unless previously irradiated
PDQ ORAL DISEASE
Fibrous Hyperplasia: Denture-Related (Epulis Fissurata)
Etiology • Trauma resulting from an ill-fitting denture • Exuberant fibrous tissue repair secondary to repeated inflammation and trauma Clinical Presentation • Found on vestibular mucosa, usually at facial aspect of denture flange • Rounded folds of broadly based fibrous tissue surrounding the overextended denture flange • Ulceration often noted at depth of tissue folds • More common in anterior segment of the jaws • May occur on hard palate as a polypoid or leaf-like mass Diagnosis • Location and presence of a chronically ill-fitting denture Differential Diagnosis • Lymphoma • Soft tissue tumor • Metastatic tumor Treatment • Excision of all tissue • Relining or reconstruction of new dentures after excision Prognosis • No recurrence anticipated with properly fitting denture
Connective Tissue Lesions
PDQ ORAL DISEASE
Florid Osseous Dysplasia (Florid Cemento-osseous Dysplasia)
Etiology • Unknown • Strong predilection for middle-aged to elderly black females Clinical Presentation • Bilateral and symmetric mandible involvement • Body and posterior segment of mandible chiefly involved • Usually asymptomatic Radiographic Findings • Early stage is mostly a radiolucent process. • Later stages have multiple, mixed, radiolucent to radiopaque nodularities. • Purely lucent areas representing simple bone cysts may be seen in conjunction with opacities. Diagnosis • Radiographic appearance • Involved teeth are vital. Differential Diagnosis • Chronic, diffusing, sclerosing osteomyelitis • Fibrous dysplasia • Osteosarcoma • Paget’s disease Treatment • In uncomplicated, asymptomatic cases, observation only • If symptomatic, surgical removal of calcified masses with concomitant antibiotic coverage • Bone saucerization and open packing may hasten progress. Prognosis • Good • When infected, osteomyelitis-related morbidity occurs.
Connective Tissue Lesions 171 .
epidermoid cysts of skin • Gene is located on chromosome 5q Clinical Presentation • Early clinical indicators may be osteomas of jaws and facial bones. • Multiple odontomas may be noted. • Prophylactic colectomy as all patients ultimately develop colon adenocarcinomas • Genetic counseling Prognosis • Relates to colon adenocarcinoma development and behavior . opaque masses • Endosteal or periosteal origin • Impacted and supplementary teeth are usually noted. colonic and rectal polyposis. cutaneous and mesenteric fibromas. sclerotic.172 PDQ ORAL DISEASE Gardner’s Syndrome Etiology • Autosomal-dominant condition • Association of multiple osteomas. facial bone osteomas • Concomitant polyposis of colon Differential Diagnosis • Exostoses of mandible/maxilla Treatment • Osteoma treatment is elective/cosmetic. • Facial asymmetry • Multiple impacted teeth and odontomas not uncommon Radiographic Findings • Well-defined. Diagnosis • Family history • Multiple jaw bone. • Colorectal polyps usually develop after osteomas.
Connective Tissue Lesions 173 .
perforation. • Can displace teeth. • Usually anterior to molar teeth • Most cases are nonaggressive. and rapid enlargement. borders may be scalloped. rarely in facial bones • Occurrence in mandible predominates 3:1 over that in maxilla. occasionally unilocular. less commonly it resorbs tooth roots • Wide size variation at time of presentation Diagnosis • Incisional biopsy • Primary hyperparathyroidism should be ruled out. slow growing. radiolucency • Margins are usually well defined.174 PDQ ORAL DISEASE Giant Cell Granuloma Etiology • Probably reactive or responsive in nature • Speculation suggests it may represent a developmental anomaly. with no cortical breakthrough or root end resorption. Differential Diagnosis • Odontogenic lesions • Ameloblastoma • Odontogenic myxoma • Odontogenic keratocyst • Nonodontogenic lesions • Hemangioma • Aneurysmal bone cyst • Traumatic bone cyst . • No radiographic or histologic features can be used to separate nonaggressive lesions from aggressive lesions. Clinical Presentation • Bony expansion • Most cases arise in those less than 30 years of age • Female predominance • Near exclusivity in mandible or maxilla. and asymptomatic. • Some cases are recurrent and exhibit aggressive behavior with pain. Radiographic Findings • Usually multilocular.
Prognosis • Aggressive variant has high recurrence rate • Generally good . if aggressive or recurrent • Calcitonin may be successful in some cases.Connective Tissue Lesions 175 • Hyperparathyroidism • Giant cell tumor Treatment • Thorough curettage • Marginal resection. • Intralesional corticosteroid placement in small lesions may be successful.
” Treatment • Identification and elimination of cause. or MurrayPuretic-Drescher. cyclosporine. Cross. Prognosis • Good • Often requires repeated excision . • May be secondary to leukemic infiltrate Clinical Presentation • Bulky enlargement of free and attached gingiva • Blunted interdental papillae • Soft and boggy to firm and dense in texture • Pink to reddish blue Diagnosis • Medical history • Biopsy Differential Diagnosis • See “Etiology. calculus) • May be related to hormonal changes (pregnancy. Rutherfurd’s. including phenytoin. puberty) • May be associated with drug use. if possible • Gingivoplasty and improvement of oral hygiene may be indicated in some cases. calcium channel blockers (especially nifedipine) • A familial form exists • Some cases may be related to Cowden disease and syndromes such as Zimmerman-Laband.176 PDQ ORAL DISEASE Gingival Hyperplasia: Generalized Etiology • May be nonspecific and reactive to local factors (plaque.
Connective Tissue Lesions 177 .
rarely pedunculated Diagnosis • Biopsy Differential Diagnosis • Traumatic fibroma • Salivary gland tumor • Neurofibroma • Other soft tissue neoplasm (eg.178 PDQ ORAL DISEASE Granular Cell Tumor (Granular Cell Myoblastoma) Etiology • A benign neoplasm. probably derived from a Schwann cell precursor Clinical Presentation • Most common site is the tongue • Wide age range • Nontender. lipoma) Treatment • Excision Prognosis • Recurrence is rare. sessile mass. rhabdomyoma. covered with intact epithelium • Usually dome-shaped. asymptomatic submucosal mass. • Rarely multiple tumors .
Connective Tissue Lesions 179 .
environmental factors Clinical Presentation • Oral expression most common with myelomonocytic and myelocytic forms. syndromic association.180 PDQ ORAL DISEASE Leukemia Etiology • Unknown • Probably multifactorial: genomic instability including genetic predisposition. coarse marrow spaces and trabeculae • Alveolar bone destruction • Loss of lamina dura and border of developmental dental crypts • Periosteal reaction with “onion skin” effect Diagnosis • Peripheral blood analysis • Bone marrow biopsy analysis Differential Diagnosis • Medication-induced gingival hyperplasia • Idiopathic thrombocytopenia • Lymphoma Treatment • Chemotherapy regimen(s)—these vary with form of disease • Bone marrow transplantation Prognosis • Varies with form of disease and response to treatment . ecchymosis • Spontaneous gingival hemorrhage • Mucosal ulceration (neutropenic ulcers) • Cervical lymphadenopathy • Loose teeth (due to infiltration of periodontal ligament) Radiographic Findings • Osteolytic lesions in up to one-half of childhood cases • Expanded. prior chemotherapy. followed by lymphocytic form • Petechiae.
Connective Tissue Lesions 181 .
Clinical Presentation • No symptoms • Discovered incidentally Radiographic Findings • Round to ovoid radiolucency below inferior alveolar canal. The depression created produces characteristic radiographic findings. recognition only Prognosis • Excellent . above inferior border. Static Bone Cyst) Etiology • Developmental depression of the lingual side of the mandible • The aberrant lobe of the submandibular salivary gland and/or adipose tissue fills the body of mandible defect.182 PDQ ORAL DISEASE Lingual Bone Defect (Stafne Bone Cyst. and below third molar area • Well defined by a dense hypercorticated margin • Size range of 1 to 3 cm • Rarely noted in premolar and canine areas Diagnosis • Radiographic appearance Treatment • None.
Connective Tissue Lesions 183 .
184 PDQ ORAL DISEASE Lingual Thyroid Etiology • Failure of thyroid primordium to descend from foramen cecum into anterior neck Clinical Presentation • Midline mass at foramen cecum area • Dark. Diagnosis • Clinical appearance. location • Demonstration of activity with radionuclide scan (technetium 99m) • Confirmation of presence of cervical thyroid Differential Diagnosis • Thyroglossal duct cyst • Squamous cell carcinoma • Lymphoma Treatment • Removal if functional thyroid is present in usual location • Move/transplant to alternative site if other thyroid tissue does not exist Prognosis • Excellent . well vascularized • May interfere with swallowing and breathing in infancy • Bleeding may occur.
Connective Tissue Lesions 185 .
pleomorphic. sessile. tongue. slow-growing. Diagnosis • Mature fat cells in lobular pattern • Usually well circumscribed by thin fibrous capsule • Several microscopic variations including infiltrating. myxoid. angioid. and spindle cell types Differential Diagnosis • Other soft tissue tumor • Minor salivary gland neoplasm • Metastatic disease Treatment • Excision Prognosis • Recurrence rare with exception of infiltrating and intramuscular types . floor of mouth • May be deep seated with no color alteration • Yellowish.186 PDQ ORAL DISEASE Lipoma Etiology • A benign neoplasm of adipose cells • Uncommon in the oral cavity Clinical Presentation • Asymptomatic. usually circumscribed. or pedunculated • Soft and compressive with doughy consistency • Most common sites include buccal mucosa. lobulated quality when superficially located • Surface of larger lesions often is covered by telangiectatic vessels.
Connective Tissue Lesions 187 .
may cause splaying of teeth and scalloping of tongue borders. tuberculosis. deep fungal infections) • Congenital disease (muscle hypertrophy or lymphangioma) • Metabolic alteration (amyloidosis) • Endocrine-related condition (acromegaly) • Neoplasia/hamartomatous condition (neurofibromatosis) Clinical Presentation • Usually diffuse enlargement. infectious forms may be asymmetric and focal • Transient forms often arise quickly. from excellent to fair . deglutition) Diagnosis • Biopsy Differential Diagnosis • See “Etiology. • Persistent forms evolve slowly.” Treatment • Management is related to etiology and extent of involvement • Surgical reduction in certain cases Prognosis • Related to etiology. and may result in functional problems (speaking.188 PDQ ORAL DISEASE Macroglossia Etiology • Macroglossia is a clinical sign caused by one of the following many conditions: • Angioedema/allergic reaction • Infection/abscess formation • Inflammation related to trauma • Granulomatous disease (sarcoidosis. swallowing.
Connective Tissue Lesions 189 .
evenly contoured • Emphasized when muscle is contracted (ie. symmetric. ? cytomegalovirus) • Autoimmune condition (Sjögren’s syndrome) • Neoplastic infiltration Treatment • Dependent upon etiology • Usually relates to defining cause and includes the following: • Observation • Management of underlying cause when appropriate Prognosis • Excellent .190 PDQ ORAL DISEASE Masseteric Hypertrophy Etiology • Usually secondary to hyperfunction (habitual) • May be related to dystrophic or metabolic disease of muscle • May be idiopathic Clinical Presentation • Usually bilateral masseter muscle enlargement • Painless. jaw is clenched) • Responds to functional or hyperfunctional demands Diagnosis • History • Muscle biopsy if metabolic disease suspected Differential Diagnosis • Sialoadenosis • Parotid gland enlargement • Bacterial infection • Viral infection (mumps.
Connective Tissue Lesions 191 .
thickened mucosa of cheeks and tongue may be seen. intralesional corticosteroid injections • Tapering dose of systemic corticosteroids • Clofazimine in slowly tapering dosage • Dapsone and other nonsteroidal anti-inflammatory drugs Prognosis • Generally good • May be persistent . • Gingival surface granularity may be present uncommonly. Diagnosis • Biopsy • Key feature is noncaseating epithelioid granulomas with multinucleated giant cells • Patch testing for contact allergy Differential Diagnosis • Angioedema • Sarcoidosis • Cellulitis/erysipelas of lip Treatment • If necessary.192 PDQ ORAL DISEASE Melkersson-Rosenthal Syndrome Etiology • A chronic. sarcoidosis. • “Correctable” causes must be excluded before an idiopathic cause is accepted. idiopathic condition • Part of orofacial granulomatosis spectrum that includes Crohn’s disease. cheilitis granulomatosa Clinical Presentation • Classic triad • Chronic intermittent swelling of lip(s) or oral tissues • Fissured tongue • Facial nerve palsy (20%) • Occasionally manifests as painless labial swelling (granulomatous cheilitis/Miescher’s granuloma) • May be seen in association with intestinal Crohn’s disease • Lobulated.
Connective Tissue Lesions 193 .
prominent lips and frenula • Conjunctival neuromas. lips. corneal nerves • Oral mucosal neuromas: tongue.194 PDQ ORAL DISEASE Mucosal Neuroma Etiology • A component of the multiple endocrine neoplasia syndrome type III (MEN III). cheeks. commissures • Marfanoid facies and habitus • Medullary thyroid carcinoma • Oral mucosal neuromas may be initial sign of syndrome Laboratory Findings of MEN III • Increased serum calcitonin levels • Increased urinary vanillylmandelic acid Microscopic Findings of Mucosal Neuroma • Plexiform bundles of neural tissue • Axons within bundles Diagnosis • Confirmation of neuroma presence • Demonstration of increased serum calcitonin Differential Diagnosis • Neurofibromatosis Treatment • Thyroidectomy • Follow-up for pheochromocytoma development • Genetic counseling . (also called type 2b) • Syndrome is related to proliferation of neural crest derivatives. as follows: • Medullary carcinoma of thyroid • Pheochromocytoma • Mucosal neuromas • Ganglioneuromatosis of the bowel • Autosomal-dominant transmission • Gene is located on chromosome 10 Clinical Presentation of MEN III • Thickened.
Connective Tissue Lesions 195 Prognosis • Guarded. with 100% risk of medullary carcinoma • 50% risk of pheochromocytoma .
buccal mucosa. • Syndromic form associated with autosomal-dominant inheritance pattern due to mutation of NF1 or NF2 genes Clinical Presentation • Tongue.196 PDQ ORAL DISEASE Neurofibroma Etiology • A benign neoplasm of peripheral nerve • Concomitant proliferation of perineural fibroblasts and Schwann cells • Multiple lesions suggest neurofibromatosis syndrome. mucobuccal fold most common sites • Soft tissue findings: discrete nodules or diffuse lobular lesions • Skin lesions with syndromic forms: café-au-lait macules. (characteristically six or more). uniform pigmentation with smoothly contoured borders Radiographic Findings (When Intrabony Lesions Are Present) • “Blunderbuss” expansion of inferior alveolar foramen • Uniformly expanded alveolar canal in body of mandible Microscopic Findings • Usually unencapsulated mass of spindle cells with gently wavy to twisted nuclei • Stromal background is delicately fibrillar • Scattered mast cells in lesions Diagnosis • Microscopic findings Differential Diagnosis • Localized neurofibroma • Neuroma • Fibroma • Widespread neurofibroma • MEN 2b/III • Proteus syndrome .
and treatment directed toward function and/or esthetics Prognosis • When isolated. up to 15% risk of malignant transformation to neurogenic sarcoma .Connective Tissue Lesions 197 Treatment • When solitary. excellent • When syndrome related. excision • When multiple. verification of the diagnosis.
Radiographic Findings • Initially ill-defined. in later phases of uncontrolled or advanced cases: • Vertigo. • Maxilla predominates over mandible by 2:1 • Jaw and skull enlargement common • Often deep aching pain in affected bone(s) • Neurologic complications. Laboratory Findings • Increased serum alkaline phosphatase • Serum calcium and phosphate normal • Elevated urinary calcium and hydroxyproline levels . • Maxillary and mandibular involvement is usually bilateral and symmetric.198 PDQ ORAL DISEASE Paget’s Disease Etiology • Unknown. often multiple lytic lesions noted • Later stage shows patchy radiopaque pattern (like cotton wool) • Hypercementosis recognizable by “drumstick” appearance of root outline • Lamina dura–periodontal membrane space may become obliterated. although several theories exist including the following: • Inborn error of connective tissue metabolism • Paramyxovirus or slow virus infection • Autoimmune-mediated vascular disorder • Possible association with alterations involving chromosomes 6 and 18 • Familial form exists Clinical Presentation • Nearly one-fifth of cases involve the mandible and maxilla. headache • Auditory/visual disturbances • Facial paresis • Monostotic involvement occurs but rarely • Dental patients often complain of ill-fitting prostheses or slow separation of teeth. as follows.
and prominent blood vessels • Late phase (sclerotic) has predominantly osteoblastic function. which results in dense bone with numerous reversal lines Diagnosis • Radionuclide imaging to determine extent and distribution of lesions Differential Diagnosis • Osteosarcoma • Fibrous dysplasia • Acromegaly Treatment • Bisphosphonate therapy • Calcitonin • Pain control Prognosis and Complications • Slowly progressive • Deformities and neurologic complications in late phases • Malignant transformation may occur (osteosarcoma) in 1% of cases. fibrous tissue replacement of bone. secondary to loss of heterozygosity in chromosome 18q.Connective Tissue Lesions 199 Microscopic Findings • Early phase predominantly has osteoclastic resorption. .
noncorticated border • Less than 1 cm in diameter • Lamina dura usually lost • With aging. usually anterior • May involve apices of one or more teeth • Noted usually in fourth and fifth decades • Associated teeth are always vital.200 PDQ ORAL DISEASE Periapical Cemento-osseous Dysplasia Etiology • A dysplastic lesion of periodontal membrane origin with no known cause Clinical Presentation • An asymptomatic focus of periapical alteration in the mandibular region. radiodensity increases Diagnosis • Radiographic features • Associated tooth (teeth) is vital Differential Diagnosis • Multiple periapical abcesses • Florid osseous dysplasia Treatment • None. Radiographic Findings • Initially. findings of a periapical radiolucency include the following: • Well-defined. observation only Prognosis • Excellent .
Connective Tissue Lesions
PDQ ORAL DISEASE
Etiology • Autoimmune, with local and systemic or multiorgan effects secondary to excessive collagen deposition • Localized sclerosis (morphea) is a distinct disorder sharing only histologic features with systemic sclerosis. Clinical Presentation • Oral findings in progressive systemic sclerosis are as follows: • Limited oral opening (microstomia) • Narrowing of lips (“purse string” sign) • Raynaud’s phenomenon (an early finding) • Facial skin becomes taut and mask-like. • Tongue becomes “bound down” and hypomobile. • Telangiectases over facial skin, lips, tongue Radiographic Findings • Prominent antegonial notch on panoramic radiograph • Variable resorption of condyles and coronoid processes • Uniform widening of periodontal membrane space • Root resorption Diagnosis • Clinical features • Microscopic features of skin or mucosal biopsy • Serology: demonstration of anticentromere antibodies or antitopoisomerase I (anti-Scl 70) Differential Diagnosis • Lichen sclerosus • Submucous fibrosis • Postradiation scarring Treatment • Systemic corticosteroids • Immunosuppressive agents • Vasodilators
Connective Tissue Lesions
• Systemic d-penicillamine • Control of local effects of disease Prognosis • Dismal for systemic form
PDQ ORAL DISEASE
Torus: Palatal and Mandibular
Etiology • Focal cortical bone overgrowth of unknown cause Clinical Presentation • Palatal: slow-growing, asymptomatic, paramedian, nodular bony mass • Mandibular: bilateral, smooth and lobular bony masses along lingual surface in cuspid-premolar area • Larger lesions may interfere with function or dental prosthesis. • Larger lesions may show surface ulceration and may lead to focal osteomyelitis. Microscopic Findings • Dense hyperplastic cortical bone with few marrow spaces Diagnosis • Clinical presentation is usually diagnostic. • Microscopic findings Treatment • Observation • Surgical removal under the following conditions: • If there is interference with seating of prosthesis • If condition is excessive or symptomatic Prognosis • Excellent
Connective Tissue Lesions
PDQ ORAL DISEASE
Salivary Gland Diseases
Etiology • Extravasation type • Physical-traumatic injury to minor gland excretory duct • Mucus extravasation into periductal soft tissue produces a local inflammatory response and granulation tissue “encapsulation.” • Variant • Superficial mucocele • Mucus pool at epithelial–connective tissue junction • Possibly trauma or systemic (hormonal) etiology Clinical Presentation • Lower lip most common site; also buccal mucosa, anterior ventral tongue • Painless bluish hue when mucin is near surface • Often waxes and wanes in size Microscopic Findings • Mucus pool surrounded by granulation tissue • Macrophage and neutrophil response to free mucin • Focal chronic sialadenitis Diagnosis • Presentation • Microscopic findings Differential Diagnosis • Hemangioma/varix • Pyogenic granuloma • Salivary neoplasm • Connective tissue neoplasm
Salivary Gland Diseases
Treatment • Excision with associated local minor salivary glands Prognosis • Occasional recurrence
especially mucoepidermoid carcinoma Treatment • Excision of cyst with adjacent gland(s) Prognosis • Recurrence is rare. dilated. epithelial-lined salivary excretory duct • Lining is cuboidal to columnar with occasional mucus-producing cells present • Adjacent salivary gland lobules minimally altered but may show obstructive inflammatory changes Diagnosis • Microscopic findings Differential Diagnosis • Extravasational mucocele • Salivary gland neoplasm.208 PDQ ORAL DISEASE Mucus Retention Cyst Etiology • Represents dilatation of salivary excretory duct due to obstruction • Duct obstruction may be due to a mucous plug or sialolith formation Clinical Presentation • Major or minor salivary glands affected in adulthood • Asymptomatic. soft mucosal swelling • Can occur at any intraoral minor salivary gland site. . especially upper lip Microscopic Findings • Thin.
Salivary Gland Diseases 209 .
• May extend to and involve deep soft tissue and palatal bone Microscopic Findings • Salivary gland inflammation and lobular necrosis (necrosis is not always demonstrable on biopsy) • Ductal squamous metaplasia (bland cytology) • Lobular architecture of salivary glands persists Diagnosis • Microscopic findings Differential Diagnosis • Salivary gland neoplasm • Squamous cell carcinoma • Granulomatous disease Treatment • Follow-up only Prognosis • Excellent . or it may appear spontaneously Clinical Presentation • Both major and minor salivary glands can be affected. • Hard palate most common site. a central necrotic crater develops.210 PDQ ORAL DISEASE Necrotizing Sialometaplasia Etiology • Local ischemic injury of salivary gland lobules • May be preceded by trauma or local anesthetic injury. usually unilateral • Initially a painful to dysesthetic submucosal swelling • Ultimately.
Salivary Gland Diseases 211 .
extravasation of saliva into the soft tissue of the floor of the mouth Clinical Presentation • Unilateral. fluctuant. soft tissue mass on the floor of the mouth • Usually has a bluish.212 PDQ ORAL DISEASE Ranula Etiology • Obstruction of the sublingual (usually) or submandibular salivary gland by a sialolith or by trauma • Secondary to obstruction. slightly translucent quality • When above the mylohyoid muscle. Diagnosis • Demonstration of sialolith • Soft tissue imaging (T2-weighted magnetic resonance image) • Aspiration of mucinous salivary fluid • Excised tissue with granulation tissue lining around mucin pool Differential Diagnosis • Dermoid cyst • Salivary gland tumor • Soft tissue tumor • Cystic hygroma • Thymic cyst Treatment • Marsupialization as an initial procedure • Excision of the involved gland (extravasation type) • Sialolithectomy (in obstructive type) Prognosis • No recurrence with sialadenectomy • Recurrence risk with sialolithectomy secondary to duct scarring or reformation of stone . • Occlusal radiographs may demonstrate a suspected sialolith. a plunging ranula forms. presentation is intraoral. • If extravasation extends below the mylohyoid muscle.
Salivary Gland Diseases 213 .
and others Clinical Presentation • Excess saliva resulting in drooling • Angular cheilosis • Diffuse parotid/submandibular salivary gland enlargement Diagnosis • Direct observation and analysis of history • Flow-rate measurement Differential Diagnosis • See “Etiology. if possible. may include idiopathic paroxysmal sialorrhea. an alternate medication should be chosen.” Treatment • Scopolamine • If related to medication use. parkinsonism. stomatitis (acute). Prognosis • Guarded/indeterminate . neostigmine. newly inserted oral appliances. expectorants.214 PDQ ORAL DISEASE Sialorrhea (Sialosis) Etiology • Varied.
Salivary Gland Diseases 215 .
postulations include the following: • Potential role for viruses/retroviruses as cofactors • Possible role of cytokine and hormonal influence on signal transduction and secretion Clinical Presentation • Decrease in exocrine gland function • Xerostomia • Xerophthalmia/keratoconjunctivitis sicca • Salivary and lacrimal gland enlargement (one-third of cases) • Secondary effects of exocrine dysfunction are as follows: • Dental caries • Oral candidiasis • Ocular/corneal discomfort • Primary form: exocrine dysfunction dominates • Secondary form: exocrine dysfunction. demonstration of presence of periductal lymphocytic sialadenitis Differential Diagnosis (Xerostomia/Parotid Gland Swelling) • Sarcoidosis • Depression • Human immunodeficiency • Autonomic neuropathy virus–associated • Graft-versus-host disease exocrinopathy • Bulimia • Drug side effects • Alcoholism • Lymphoma • Diabetes mellitus .216 PDQ ORAL DISEASE Sjögren’s Syndrome Etiology • An autoimmune disease resulting in exocrine gland dysfunction secondary to mononuclear cell infiltration • Increased prevalence of human leukocyte antigen DR/DQ alleles • Autoantibody production against nuclear antigens SS-A and SS-B • No specific agent identified. other associated autoimmune conditions—usually rheumatoid arthritis. less often lupus erythematosus Diagnosis • Demonstration of objective xerostomia and xerophthalmia • Serologic demonstration of associated SS-A or SS-B antibodies • Correlation of clinical and serologic findings with labial salivary gland biopsy.
including the following: • Reduction of oral dryness • Pilocarpine • Cemiveline • Oral moisturizing agents (saliva substitutes) • Gustatory stimulation • Ocular moisture replacement • Saline • Synthetic glycoprotein solutions • Carboxymethylcellulose sodium • Ocular punctual occlusion • Frequent dental/ophthalmic examinations Prognosis • Guarded • High risk of lymphoma compared with risk in those without autoimmune disease .Salivary Gland Diseases 217 Treatment • Directed at associated connective tissue or autoimmune disease • Systemic corticosteroids if acute symptoms arise • Usually symptomatic and preventative therapies are used.
P53. and others • Causative association with Epstein-Barr (EB) virus. causing malocclusion and/or exfoliation. chiefly of the mandible • Proptosis in children may occur in association with maxillary lesions. • Scattered macrophages with abundant pale cytoplasm contain- .218 PDQ ORAL DISEASE Lymphoid Lesions Burkitt’s Lymphoma Etiology • B lymphocyte malignancy associated with genetic mutations: C-MYC. Diagnosis • A diffuse proliferation of small noncleaved lymphoid cells (B lymphocyte–derived cells) • Tumor cells have round nuclei and prominent nucleoli. • Pain and paresthesia associated with jaw lesions • Children predominately affected • Facial presentation noted in 25% of North American (nonendemic) cases. North American form less strongly associated Clinical Presentation • Rapidly progressive facial asymmetry. nearly 100% in African children (endemic cases) • Abdominal (retroperitoneal) presentation usually noted initially in nonendemic form and in a wider age range than in endemic form Radiographic Findings • Ill-defined radiolucency • Loss of lamina dura and developmental crypt(s) around unerupted teeth • Uniform widening of periodontal membrane space • Teeth may be displaced. and malaria cofactor believed to increase the risk for gene-translocation accidents • African form closely associated with EB infection.
high-dose fractionated therapy Prognosis • Fair . osteosarcoma) • Acute infection Differential Diagnosis: Microscopic • Other round cell malignancies of childhood (neuroblastoma.Lymphoid Lesions 219 ing pyknotic cellular debris represent the “stars” in the socalled starry sky appearance. leukemia. Differential Diagnosis: Clinical • Other jaw malignancies of childhood (Ewing’s sarcoma. embryonal rhabdomyosarcoma) Treatment • Multiagent chemotherapy • Overall cure rate in children is now up to 90% with intensive.
220 PDQ ORAL DISEASE Lymphoepithelial Cyst Etiology • Entrapment of oral mucosal epithelium within lymphoid tissue in foliate papillae. floor of the mouth. soft palate Clinical Presentation • Yellow to white nodule • Asymptomatic. ventral tongue. slow growing • May drain or decompress spontaneously • Most common in second then fourth decades • Overlying mucosa intact. smooth Diagnosis • Histologic demonstration of lymphoid tissue with germinal centers surrounding true cyst lumen filled with epithelial debris Differential Diagnosis • Lipoma • Minor salivary gland neoplasm or sialolith • Mucocele Treatment • Excision Prognosis • Excellent .
Lymphoid Lesions 221 .
depending upon type/subtype: cell size. immunohistochemical studies • Flow cytometry • Staging work-up involves the following: • Bone marrow biopsy • Whole body computed tomography scan Differential Diagnosis • Salivary neoplasm • Metastatic tumor . maturation level • Classification schemes dependent upon microscopic features • Human immunodeficiency virus–associated lymphomas are typically diffuse. large cell. gingiva. pain • Paresthesia of lip when occurring in mandible • Initial presentation in oral cavity is uncommon (2%) • Predominant oral sites: palate.222 PDQ ORAL DISEASE Lymphoma Etiology • Idiopathic • Long-term immunosuppression • ?Post radiation Clinical Presentation • Relatively common in head and neck region • Most common in middle-aged and older individuals • Mass of reddish blue tissue with ulceration. • Revised European American Lymphoma Classification and Working Formulation are current microscopic classifications Diagnosis • Biopsy. buccal mucosa. mandible • May arise within lymph nodes or extranodally in soft tissue • Ill-defined radiolucency in bone • Hodgkin’s lymphoma rare in oral cavity • Burkitt’s lymphoma arises in children. pattern. high-grade lymphomas. almost always B cell type • Varied. • EB virus is often evident in tumor cells. Microscopic Findings • Non-Hodgkin’s lymphoma predominates.
Lymphoid Lesions 223 • Soft tissue tumor (primary) • Leukemia Treatment • Dependent upon extent/clinical stage and microscopic features • For localized (stage I) disease: radiation therapy • Chemotherapy or combined chemotherapy-radiation therapy for more widespread disease • Very-low-grade lesions may be observed only since treatment typically has no effect on outcome. acquired immunodeficiency syndrome–associated lymphoma has a poor outcome • Very-low-grade lesions have excellent prognosis . Prognosis • Dependent upon clinical stage and histologic subtype.
Radiographic Findings • Sharply defined radiolucencies.224 PDQ ORAL DISEASE Myeloma Etiology • Neoplastic proliferation of malignant plasma cells • Monoclonal immunoglobulin (κ or λ light chain) production Clinical Presentation • Occurs exclusively in adulthood (males 2:1 over females) • Bone pain and paresthesia • Mucosal involvement may occur as polypoid to lobular masses. • Purpura and woody induration of the tongue (macroglossia)or gingiva may be the initial manifestation. • Solitary presentation invariably becomes multiple myeloma. diffuse plasma cell proliferation • Variable levels of differentiation and mitotic activity • Immunohistochemical demonstration of monoclonality (κ or λ light chains) Diagnosis • Biopsy • Immunohistochemical evaluation Differential Diagnosis • Lymphoma • Primary osseous tumor • Metastatic tumor • Traumatic bone cyst . • The extramedullary form occasionally becomes multiple myeloma. usually of many bones • Absence of marginal hyperostosis or opaque lining Laboratory Findings • Monoclonal gammopathy by serum electrophoresis • Bence Jones proteinuria • Plasma cells in bone marrow aspirate Microscopic Findings • Monotonous.
Lymphoid Lesions 225 Treatment • Chemotherapy • Local radiation therapy Prognosis • Poor .
multiloculated. destructive bony lesion • Surrounding bone may be sclerotic • Angiogram demonstrates intense vascularity Diagnosis • Radiographic lytic lesion • Honeycombed quality of large vascular sinusoidal spaces and bony septa • May be confused microscopically with central giant cell granuloma Differential Diagnosis • Ameloblastoma • Odontogenic keratocyst • Odontogenic myxoma • Hemangioma • Giant cell granuloma Treatment • Excision to en bloc resection Prognosis • Good to excellent . stabilization Clinical Presentation • Bony expansion and occasionally mild pain • Chiefly occurs in mandible • Female predilection Radiographic Findings • Expansile.226 PDQ ORAL DISEASE Cysts Aneurysmal Bone Cyst Etiology • Unknown • Possibly represents a vascular response/repair to jaw injury (an arteriovenous malformation) • Three phases: incipient. destructive.
Cysts 227 .
stimulus unknown Clinical Presentation • Usually a unilocular. Diagnosis • Stratified squamous lining with prominent basal layer • Budding or extension of epithelium into the cyst wall may be noted. chiefly of maxilla • Scattered opacities seen in up to 50% of cases • May be associated with the crown of an unerupted tooth • An extraosseous form may occur (usually anterior to first molar) • May be more solid than cystic (odontogenic ghost cell tumor) Radiographic Findings • Well-defined radiolucency or lucency with opaque foci (dystrophic calcification of keratin produced by lining epithelium) • Tooth displacement or root resorption may be seen. Differential Diagnosis: Radiographic • Calcifying epithelial odontogenic tumor • Ossifying fibroma • Ameloblastic fibro-odontoma . • Foreign body reaction may occur when ghost cells come in contact with connective tissue. well-defined radiolucency.228 PDQ ORAL DISEASE Calcifying Odontogenic Cyst Etiology • An odontogenic cyst with characteristic microscopic pattern • May be noted in association with other odontogenic tumors • Origin is residual odontogenic epithelium in the jaws. • Characteristic ghost cell keratinization required for diagnosis • Ghost cells may undergo dystrophic calcification. • The solid or tumorous form shares microscopic features with ameloblastoma.
Cysts 229 Treatment • Enucleation/excision • If noted in association with another odontogenic tumor. consideration must be given to the behavior of the accompanying lesion. especially in association with solid lesions • Overall prognosis is very good • Excellent prognosis for peripheral (gingival) lesions . Prognosis • Some recurrence potential.
parakeratinized epithelial lining with keratinfilled cyst cavity is noted. yellow-white nodules over the alveolar crest in neonates • Usually involute following spontaneous cyst rupture Diagnosis • Appearance and location • Histologically. Gingival Cyst of Newborn) Etiology • Cystic degeneration of residual dental lamina/odontogenic epithelium • Found in over 80% of newborns Clinical Presentation • Small (1–2 mm). Differential Diagnosis • Eruption cyst Treatment • None.230 PDQ ORAL DISEASE Dental Lamina Cyst (Bohn’s Nodules. usually multiple. observation only Prognosis • Excellent .
Cysts 231 .
cortex is thinned and rarely perforated Radiographic Findings • Well-defined radiolucency enclosing crown of unerupted tooth • Corticated/opaque margins unless infected • May produce root resorption of adjacent erupted teeth • Usually unilocular.232 PDQ ORAL DISEASE Dentigerous Cyst Etiology • A developmental odontogenic cyst arising subsequent to separation between dental follicle and the crown of an associated unerupted tooth • Proliferation of reduced enamel epithelium lining the follicle. degeneration of the stellate reticulum component of the enamel organ occurs during odontogenesis. cuboidal. followed by maxillary canines • Usually noted during second and third decades • Asymptomatic. nonkeratinized epithelial lining two cell layers thick with flat epithelial–connective tissue interface • Loosely arranged collagen bundles. with fluid accumulation between epithelium and impacted tooth crown • Alternatively. nonkeratinized squamous epithelial lining with epithelial ridge development • Variable chronic inflammatory cell infiltrate within condensed collagen stroma . Clinical Presentation • Most commonly involves frequently impacted teeth: mandibular third molars. less commonly multilocular Diagnosis: Microscopic • Cysts without secondary inflammation • Thin. discovered on routine radiographic examination • Painless jaw/alveolar expansion may occur. occasionally containing scattered odontogenic epithelial rests • Cysts with secondary inflammation • Hyperplastic.
rarely.Cysts 233 Differential Diagnosis: Radiographic • Odontogenic keratocyst • Ameloblastoma Treatment • Cyst enucleation and extraction of associated tooth • Marsupialization prior to excision may be considered if the cyst is very large. squamous cell carcinoma) . Prognosis • Excellent • Possible complications • Pathologic fracture with large lesions • Neoplastic transformation of epithelial lining (ameloblastoma and.
but is otherwise unremarkable • May have doughy consistency because of sebum and/or keratin in cystic cavity Microscopic Findings • Epithelial lining (stratified squamous) • Cyst contents may include keratin debris. mucus • Histologic demonstration of hair follicles.234 PDQ ORAL DISEASE Dermoid Cyst Etiology • Cystic degeneration of entrapped epithelium within the midline fusion zone between the first and second branchial arches • Alternative etiology relates to in utero traumatic epithelial implantation into floor of mouth area Clinical Presentation • Slowly enlarging. usually asymptomatic. sublingual or floor-ofmouth mass • May present as a soft and compressible paramedian swelling or deformity • Overlying mucosa/skin is thinned. sebum. sebaceous glands. keratin. hair follicles/hair. and sebaceous and sweat glands. • Rarely find gastric mucosal characteristics present in cyst lining Diagnosis • Aspiration may yield cellular debris. keratinizing cystic lining Differential Diagnosis • Cellulitis of odontogenic origin • Sublingual sialadenitis • Ranula (superficial or deep/plunging) Treatment • Intraoral surgical excision Prognosis • Excellent .
Cysts 235 .
236 PDQ ORAL DISEASE Eruption Cyst Etiology • Soft tissue cyst of attached gingiva secondary to fluid accumulation within the follicular space of an unerupted tooth Clinical Presentation • Gingival swelling on the alveolar crest • Usually soft. translucent to bluish (“eruption hematoma”) Diagnosis • Location • Radiographic demonstration of erupting tooth Differential Diagnosis • Gingival cyst Treatment • Usually none is necessary as tooth typically erupts through lesion • Possibly unroof cyst to facilitate eruption Prognosis • Excellent .
Cysts 237 .
may be expansile • Located chiefly in the anterior mandible • May present a lateral periodontal relationship Radiographic Findings • Usually a multilocular cystic radiolucency • Sharply defined with hyperostotic margins • May be extensive. locally invasive.238 PDQ ORAL DISEASE Glandular Odontogenic Cyst Etiology • A developmental odontogenic cyst • A unique jaw cyst with microscopic evidence of glandular differentiation Clinical Presentation • Slow growing. . peripheral ostectomy • En bloc excision • Primary reconstruction Prognosis • Recurrence may be associated with conservative management. may perforate cortical bone Diagnosis • Radiographic qualities • Incisional biopsy results show cystic epithelium with mucous cells and pseudoduct formation Differential Diagnosis • Giant cell lesion • Ameloblastoma • Odontogenic keratocyst • Lateral periodontal cyst Treatment • Excision.
Cysts 239 .
lateral radicular cyst • Primordial cyst/odontogenic keratocyst • Odontogenic tumor • Glandular odontogenic cyst Treatment • Conservative enucleation • The botryoid variant requires more aggressive curettage. longer-term follow-up necessary .240 PDQ ORAL DISEASE Lateral Periodontal Cyst Etiology • Stimulus unknown • Dental lamina remnant proliferation within the alveolar segment of the jaw. may be multilocular (botryoid odontogenic cyst) Diagnosis • Thin. Differential Diagnosis • Inflammatory. the lateral incisor area predominates. Radiographic Findings • Well delineated. Prognosis • Recurrence uncommon • Increased risk of recurrence with botryoid variant. nonkeratinized epithelial lining • Nodular epithelial thickening along cyst lining • Lining cells are cuboidal with interspersed clear glycogen-filled cells. opaque (corticated) margin • Located lateral to vital tooth roots • Usually unilocular. separate from the periodontal ligament Clinical Presentation • Asymptomatic • Usually occurs in fourth decade and beyond • Usually in mandibular canine/premolar region (65%) • In the maxilla. round to ovoid lucency with thin.
Cysts 241 .
nonodontogenic cyst • Cystic degeneration of epithelial remnants of the vestigial nasopalatine duct Clinical Presentation • Usually develops in adulthood • May be incidental on routine dental radiographs • Palatal mass with tenderness and drainage • Adjacent teeth are vital. or heart shaped Diagnosis • Radiographic features • Biopsy confirmation Differential Diagnosis • Apical/radicular cyst • Other odontogenic cysts • Odontogenic tumor Treatment • Enucleation Prognosis • Rarely recurs .242 PDQ ORAL DISEASE Nasopalatine Duct Cyst Etiology • Developmental. ovoid. Radiographic Findings • Well-defined. greater than 5 to 6 mm in diameter • Border usually sclerotic • Round. median-paramedian radiolucency in anterior maxillary midline.
PDQ ORAL DISEASE
Nevoid Basal Cell Carcinoma Syndrome
Etiology • Autosomal-dominant condition • Loss of heterozygosity at chromosome 9q22.3 • Mutation of PTCH tumor suppressor gene Clinical Presentation • Multiple jaw cysts (odontogenic keratocysts) • Numerous cutaneous basal cell carcinomas, which arise early in life and are independent of sun exposure • Bifid ribs • Calcification of falx cerebri • Ocular hypertelorism • Mandibular prognathism • Broad nasal bridge • Medulloblastoma • Palmar and plantar pits Radiographic Findings • Multiple jaw radiolucencies • Lamellar calcification of falx cerebri • Bifid rib on abdominal radiograph Diagnosis • Radiographic and clinical findings Differential Diagnosis • Other syndromes, such as the following: • Charcot-Marie syndrome • Waardenburg’s syndrome Treatment • Excision of basal cell carcinomas and odontogenic keratocysts • Excision of other related aggressive tumors at other sites • Genetic counseling Prognosis • Guarded
PDQ ORAL DISEASE
Etiology • A benign, aggressive developmental odontogenic cyst; may be associated with mutation of PTCH tumor suppressor gene Clinical Presentation • 5 to 15% of odontogenic cysts • Usually occurs sporadically as an isolated finding • Approximately 5% are associated with nevoid basal cell carcinoma. • 5% of patients have multiple odontogenic keratocysts (OKCs) and no syndrome Radiographic Findings • Can occur in any area of maxilla or mandible • Rarely may arise in gingival soft tissue only (peripheral) • Mandible is preferred site in 65 to 78% of cases • Often (40%) seen in a dentigerous relationship • Discrete radiolucency, usually in relation to teeth (apical, lateral radicular, pericoronal to impacted tooth) • May be unilocular to multilocular Microscopic Findings • Thin, parakeratinized epithelial lining (6–10 cells thick) • Wavy, corrugated surface configuration • Prominent, palisaded, cuboidal to low-columnar basal cell layer • Basal layer “budding” into fibrous stroma is seen occasionally • Satellite or daughter cyst formation noted frequently Diagnosis • Radiographic features • Microscopic findings Differential Diagnosis • Odontogenic cysts: dentigerous, radicular, lateral periodontal, or glandular odontogenic • Nonodontogenic cyst: nasopalatine duct • Odontogenic tumors: ameloblastoma, myxoma
• Giant cell granuloma • Central mucoepidermoid carcinoma Treatment • Excision with curettage of bony confines Prognosis • The recurrence rate varies from 10 to 30% (solitary OKCs). • Recurrence rates are greatest in patients with a syndrome.
PDQ ORAL DISEASE
Etiology • A developmental odontogenic cyst arising from cystic degeneration of the enamel organ prior to formation of hard tissue Clinical Presentation • Invariably has the microscopic appearance of odontogenic keratocyst • Rare • Radiolucent lesion of jaw • Occurs in place of a tooth, usually a third molar Radiographic Findings • A well-defined radiolucency • Most commonly in the posterior mandibular quadrants Diagnosis • Radiograph shows a cyst instead of a tooth • Histologically an odontogenic keratocyst Differential Diagnosis • Odontogenic tumor • Other odontogenic cyst • Central giant cell granuloma Treatment • Enucleation with bone curettage Prognosis • Significant recurrence rate • Long-term follow-up mandated
PDQ ORAL DISEASE
Etiology • Preceded by periapical granuloma; arises as follows: • Secondary to necrosis of dental pulpal tissue • Stimulation of epithelial network (Malassez’s rest) at tooth root apex results in cystification • Cyst growth continues secondary to effects of osmotic gradient across epithelial lining layers, mediators of inflammation, and epithelial proliferation Clinical Presentation • Asymptomatic unless there is an acute exacerbation • Usually a limited process at root apex or lateral to root surface • Radiograph shows a round and well-defined lucency, usually with a sclerotic margin. • Generally 1 cm or less across, but can be significant in size • Root resorption uncommon Microscopic Findings • Stratified squamous epithelial lining • Lumen filled with cell debris, fluid, cholesterol • Connective tissue wall with mixed inflammatory infiltrate Diagnosis • Documentation of nonvital tooth • Radiograph shows alteration of apical bone Differential Diagnosis • Periapical granuloma • Central giant cell granuloma • Odontogenic and nonodontogenic tumors • Metastatic tumor Treatment • Endodontic therapy or • Periapical surgery and biopsy or • Tooth extraction and biopsy
Prognosis • Excellent • Occasional recurrences
PDQ ORAL DISEASE
Thyroglossal Duct Cyst
Etiology • Cystic change associated with thyroglossal duct remnants that failed to involute (tenth week of development) • Rarely may be hereditary in origin (autosomal dominant or recessive) Clinical Presentation • Soft, painless, and slowly enlarging mass in anterior midline of the neck of children and young adults • Usually unilocular as seen by ultrasound examination • Mass is usually mobile • Most occur above the hyoid bone. • May involve the tongue Microscopic Findings • Cyst lining of squamous, transitional, ciliated columnar epithelium composite • The cyst wall may contain residual thyroid tissue. Diagnosis • Ultrasonography • Clinical presentation of midline neck mass • Histopathology Differential Diagnosis • Base-of-tongue carcinoma • Base-of-tongue salivary tumor • Thyroid carcinoma arising within cyst Treatment • Surgical excision Prognosis • Excellent • Recurrence owing to tortuous morphology • Rarely, carcinomatous transformation of duct lining or remnants of thyroid parenchyma are noted.
PDQ ORAL DISEASE
Traumatic Bone Cyst
Etiology • Unknown in most cases • May be due to traumatic injury producing intramedullary hemorrhage and subsequent clot resorption • Alternative theory suggests degeneration of primary intrabony pathology Clinical Presentation • Peaks in second decade • Usually in body of mandible • Painless in most cases • Swelling noted in one-fourth of cases Radiographic Findings • Clearly defined radiolucency • Margins may be uneven but clear. • May extend between tooth roots creating a scalloped pattern Diagnosis • Radiographic appearance • Clinical finding of an empty bony space (pseudocyst) • Collagen and fibrin line the dead space (no epithelium). • Lamellar bone may be noted along the bony margin. Differential Diagnosis • Central giant cell granuloma • Fibro-osseous lesion (early) • Hemangioma Treatment • Surgical exploration • Observation for resolution Prognosis • Excellent • Small risk of recurrence
Cysts 255 .
5 to 30 years. Microscopic Findings • Characteristic intraluminal/intracystic growth with welldefined capsule • Dual cell population: spindle cells and cuboidal to columnar cells forming tubules or pseudoducts • Foci of dystrophic calcification or eosinophilic droplets may be noted. Diagnosis • Radiographic features • Microscopic findings . often adjacent to crown of unerupted tooth • Opaque foci may be scattered within the lucency in a “snowflake” or “salt and pepper” pattern. unilocular.256 PDQ ORAL DISEASE Odontogenic Tumors Adenomatoid Odontogenic Tumor Etiology • Derivation from epithelial component of the enamel organ • Represents less than 10% of odontogenic tumors • Biologic behavior allows for distinction from ameloblastoma Clinical Presentation • Narrow age range. with most cases noted during second decade • Female predilection • Anterior jaw location common • Association with unerupted tooth • Asymptomatic. occasionally produces expansion of alveolar bone • Rarely occurs in gingival soft tissue (peripheral) • May produce root divergence of adjacent teeth Radiographic Findings • Well defined.
Odontogenic Tumors 257 Differential Diagnosis • Dentigerous cyst • Odontogenic keratocyst • Calcifying odontogenic cyst • Lateral root cyst • Calcifying epithelial odontogenic tumor Treatment • Enucleation Prognosis • No recurrence .
258 PDQ ORAL DISEASE Ameloblastic Fibroma and Ameloblastic Fibro-odontoma Etiology • Ameloblastic fibroma: a benign mixed odontogenic tumor with concomitant epithelial and mesenchymal neoplastic proliferation • Ameloblastic fibro-odontoma: as for ameloblastic fibroma with the addition of an odontoma • Spontaneous. dentin formation associated with odontoma (when present) Differential Diagnosis • Ameloblastoma • Dentigerous cyst • Odontogenic keratocyst • Odontogenic myxoma • Central giant cell granuloma . usually posterior region • No gender predilection • May cause jaw expansion • Asymptomatic Radiographic Findings • Well defined with hyperostotic margin • Unilocular to multilocular • Often associated with an unerupted tooth • Ameloblastic fibro-odontoma has opaque component(s) related to enamel and dentin in the odontoma component Diagnosis • Lobulated. cellular mesenchymal component with proliferating odontogenic epithelium in cords and islands • Enamel matrix. no known cause for either Clinical Presentation • Noted mostly in first and second decades • Approximately 70% in mandible.
Odontogenic Tumors 259 Treatment • Conservative surgical excision/curettage Prognosis • Excellent .
• Can expand affected jaw in any plane • Cortical perforation may occur.3 cases per million people Clinical Presentation • Peak incidence during third to fifth decades • 80% occur in the mandible.260 PDQ ORAL DISEASE Ameloblastoma Etiology • A benign. facial asymmetry • Extraosseous or peripheral variant arises in gingival tissues of older adults (fifth to seventh decades) • Typically slow growing. smooth. occurs in younger patients. Diagnosis • Sheets. aggressive jaw tumor of odontogenic epithelial (ectodermal) origin. has a less aggressive clinical course and is managed more conservatively • Malignant variants rarely seen Differential Diagnosis • Dentigerous cyst • Odontogenic keratocyst . cystic (unicystic) ameloblastoma. islands of odontogenic epithelium • Peripheral layer of cuboidal to columnar ameloblast-like cells enclosing a cell population analogous to stellate reticulum of the enamel organ • Cystic degeneration common within stellate reticulum component • Several histologic patterns described have no clinical relevance. strands. even borders • May be unilocular to multilocular • Root resorption or tooth displacement may be seen. the most common odontogenic tumor after the odontoma • Incidence of 0. • A biologic variant. chiefly in molar and ramus region • Often presents in association with unerupted third molar teeth • May produce marked deformity. but persistent Radiographic Findings • Osteolytic or radiolucent with sclerotic.
• The cystic variant requires local excision. location • Solid/multicystic lesions generally require local excision or resection. size. as recurrences may follow curettage only Prognosis • Generally good.Odontogenic Tumors 261 • Odontogenic myxoma • Central giant cell granuloma Treatment • Varies with subtype. recurrence rates higher with conservative treatment • Recurrence rates of up to 15% following marginal resection • Very good prognosis for cystic ameloblastoma • Long-term follow-up necessary .
odontogenic myxoma • With mixed radiolucent and radiopaque features: calcifying odontogenic cyst. ameloblastoma. fibro-osseous lesion. most often with mixed radiolucent and radiopaque features • Impacted tooth often obscured by tumor-associated calcification • Margins may be well defined or sclerotic and vague. and concentric calcifications with epithelial islands Differential Diagnosis • When radiolucency predominates: dentigerous cyst. Diagnosis • Radiographic features • Biopsy findings of polyhedral epithelial cells. osteoblastoma Treatment • Local. nuclear pleomorphism. conservative excision including a thin rim of normal bone (so-called ostectomy) versus conservative en bloc removal • Peripheral lesions with a narrow periphery of normal-appearing mucosa . slow growing • Mean age of occurrence is approximately 40 years • Occasional soft tissue origin (peripheral) noted as a sessile gingival mass • Jaw expansion a common clinical presentation Radiographic Findings • Usually noted in association with an impacted tooth • Multilocular. amyloid material. adenomatoid odontogenic tumor. odontogenic keratocyst. ameloblastic fibro-odontoma.262 PDQ ORAL DISEASE Calcifying Epithelial Odontogenic Tumor Etiology • A benign odontogenic tumor of uncertain histogenesis • Stratum intermedium component of enamel organ is favored cell of origin Clinical Presentation • Chiefly in posterior mandible • Painless.
Odontogenic Tumors 263 Prognosis • Very good • Recurrence rate is low. from 10 to 15% • Long-term follow-up recommended .
unilocular to multilocular radiolucency • Loculi range from small “honeycomb” to large “soap bubble” shapes • Cortical thinning may be present with larger lesions. glandular odontogenic cyst • Central giant cell granuloma Treatment • Excision with bony curettage • Large lesions may require en bloc resection. Microscopic Findings • Minimal cellularity. . • Perforation of the cortex is uncommon.264 PDQ ORAL DISEASE Odontogenic Myxoma Etiology • A benign odontogenic tumor • Unknown origin Clinical Presentation • A lesion of adulthood (average occurrence at 30 years) • Equal male:female and mandible:maxilla occurrences • Wide age range: second through sixth decades • Usually asymptomatic • May produce jaw expansion Radiographic Findings • Well-defined. myxoid background • Variable amounts of collagen • Scattered residual bony trabeculae • Odontogenic epithelial rests are rarely noted. dentigerous cyst. Diagnosis • Radiographic features • Microscopic findings Differential Diagnosis • Other odontogenic tumor: ameloblastoma • Odontogenic cysts: odontogenic keratocyst.
secondary to gelatinous quality and lack of capsule .Odontogenic Tumors 265 Prognosis • Good • Can be aggressive rarely • Recurrences not uncommon.
Radiographic Findings • Well-localized. • Presence may be heralded by an over-retained primary tooth or by alveolar swelling. cementum. dentin. usually small and discovered incidentally • Jaw expansion may be present with large lesions. may contain a few small teeth or large numbers of tiny tooth-like structures Diagnosis • Radiographic presentation • Histologic demonstration of dental hard tissues Differential Diagnosis • Ameloblastic fibro-odontoma • Adenomatoid odontogenic tumor • Calcifying odontogenic cyst • Focal sclerosing osteitis. osteoma Treatment • Conservative excision/curettage Prognosis • Excellent . and pulp tissue Clinical Presentation • Two forms. as follows: • Complex: a randomly arrayed mixture of dental tissues with no gross resemblance to a tooth • Compound: multiple. tooth-like structures • Mean age of occurrence. usually the maxilla.266 PDQ ORAL DISEASE Odontoma Etiology • A hamartomatous or benign mixed odontogenic tumor of the jaw • Composed of enamel. 12 to 16 years • Asymptomatic. mixed radiolucent and radiopaque lesion • Within alveolar segment of jaws • Complex form most commonly noted in mandibular molar area • Compound form favors anterior jaw region.
Odontogenic Tumors 267 .
• Uncommon to rare • Also seen centrally (within bone) Diagnosis • Fibrous to myxoid stromal tissue • Scattered islands and strands of odontogenic epithelium • Some cells may be vacuolated. firm. • Underlying alveolar bone is spared.268 PDQ ORAL DISEASE Peripheral Odontogenic Fibroma Etiology • A benign proliferation neoplasm of fibroblastic and odontogenic epithelial origin Clinical Presentation • Asymptomatic. • The degree of epithelial proliferation may vary from minimal to prominent. Differential Diagnosis • Peripheral giant cell granuloma • Pyogenic granuloma • Peripheral fibroma • Peripheral ameloblastoma Treatment • Excision: local and conservative Prognosis • Excellent . slow-growing mass of the attached gingiva • Overlying mucosa unremarkable and intact • Sessile growth pattern • Usually along facial or buccal aspect of gingiva • Calcifications may be present radiographically.
Odontogenic Tumors 269 .
or multicentric Clinical Presentation • Typically presents as a mass in the lateral neck • May be associated with bruit. dysphagia Diagnosis • Ultrasonography as a screening measure • Angiography of both carotid systems Differential Diagnosis • Metastatic tumor • Vagal nerve sheath tumor Treatment • Surgical removal • Radiation therapy • Combined surgical and radiotherapy Prognosis • Generally good • Can be locally invasive • May metastasize in 5 to 25% of cases . hoarseness. bilateral.270 PDQ ORAL DISEASE Benign Nonodontogenic Tumors Carotid Body Tumor Etiology • Rare neoplasm arising from nonchromaffin paraganglia in carotid artery bifurcation • Heredofamilial (autosomal-dominant) form can occur (in less than 10%) • Can be multiple.
Benign Nonodontogenic Tumors 271 .
unremarkable • Usually develops in adults Diagnosis • May appear radiographically as homogeneous opacities Differential Diagnosis • Peripheral fibroma • Periostitis • Periosteal/parosteal osteosarcoma Treatment • None required • May need to be removed for prosthesis (denture) construction Prognosis • Excellent . usually bilateral and symmetric • Usually multiple. bony.272 PDQ ORAL DISEASE Exostosis Etiology • Unknown • Probable reactive phenomenon (stimulus undetermined) Clinical Presentation • Asymptomatic. slow growing • Most commonly along buccal/facial aspects of the maxillary and mandibular alveolar ridge • Overlying mucosa intact. nodular masses • Cortical bone enlargement of the jaws.
Benign Nonodontogenic Tumors 273 .
Microscopic Findings • Prominent stromal cellularity • Woven bone and/or psammomatous calcifications • Plump osteoblast rimming Diagnosis • Correlation of histologic and radiographic findings Differential Diagnosis • Osteosarcoma • Central giant cell granuloma • Odontogenic tumor Treatment • Wide local excision or resection • Reconstruction Prognosis • Recurrence rate of 30 to 50% .274 PDQ ORAL DISEASE Juvenile Ossifying Fibroma Etiology • A rapidly evolving variant of ossifying fibroma of the young • Cause unknown Clinical Presentation • Onset between 5 and 15 years of age • Rapid growth over several weeks • Maxilla and paranasal areas predominate • Tooth displacement common Radiographic Findings • Well-defined radiolucency • Focal mineralization may be noted. • Adjacent bone may be eroded or destroyed.
Benign Nonodontogenic Tumors 275 .
gingival inflammation. bone marrow. as follows: • Unifocal or multifocal chronic disease of bone (eosinophilic granuloma) • Widely disseminated chronic disease of bone and soft tissue (Hand-Schüller-Christian disease) • Acute. sharply circumscribed • “Floating teeth” appearance with alveolar bone involvement • Skeletal survey should be performed to rule out multiple bone involvement Diagnosis • Radiographic demonstration of lytic bony lesions • Infiltrate of mononuclear cells.” Idiopathic Histiocytosis) Etiology • Unknown • Proliferation of Langerhans’ cells (immune surveillance cells) normally found in skin. including eosinophils. lymphocytes. often with clefted nuclei • Often accompanied by a variety of other cell types. • Ultrastructural demonstration of cytoplasmic racquet-shaped Birbeck granules Differential Diagnosis: Clinical • Cat-scratch disease • Juvenile xanthogranuloma . and lymph nodes Clinical Presentation • A broad spectrum. plasma cells • Immunohistochemical demonstration of CD1a staining • Langerhans’ cells also stain for S-100 protein. mucosa. • Jaw lesions noted in up to 20% of cases with tenderness. although the antibody is less specific. giant cells. and friability Radiographic Findings • Bone lesions often punched out.276 PDQ ORAL DISEASE Langerhans Cell Disease (“Histiocytosis X. disseminated disease with bone marrow involvement (Letterer-Siwe disease) • Most arise in childhood. loose teeth (focal to segmental). typically divided into three subsets. eosinophilic granuloma often arises in adolescents and adults.
vincristine. as follows: • Localized variant: very good • Disseminated variant: fair to poor .Benign Nonodontogenic Tumors 277 Differential Diagnosis: Radiologic • Juvenile periodontitis. leukemia. cyclophosphamide • Bone marrow transplantation for resistant/recurrent disease Prognosis • Varies with form of disease. endocrinopathies. bony malignancy (primary/metastatic) • In adults: myeloma Treatment • Localized variant • Surgical curettage of bony lesions • Low-dose radiation therapy of inaccessible lesions • Widespread variants • Chemotherapy including methotrexate. hypophosphatasia.
• Can resorb roots and displace teeth • May displace mandibular canal Microscopic Findings • Fibrovascular stroma • Islands/trabeculae of osteoid. malocclusion. Radiographic Findings • Well-delineated. smooth contours • Quality varies from lucent to opaque • Margins may be sclerotic. Diagnosis • Correlation of histologic and radiographic findings Differential Diagnosis: Radiographic • Odontogenic cyst • Giant cell lesion • Odontogenic tumor Differential Diagnosis: Histologic • Fibrous dysplasia (must have clinical-pathologic correlation) Treatment • Conservative excision • Enucleation with peripheral bony curettage . woven bone • Cementum droplets may be present. dysfunction • Mandibular lesions are more common than are maxillary.278 PDQ ORAL DISEASE Ossifying Fibroma Etiology • A benign fibro-osseous lesion of bone • Cause unknown Clinical Presentation • Expansile lesion of bone • Cortices intact • May produce deformity.
Benign Nonodontogenic Tumors 279 Prognosis • Excellent .
sclerotic • May be subperiosteal or medullary Diagnosis • Radiographic features • Microscopic features: normal cortical and trabecular bone Differential Diagnosis • Tori. if compromising Prognosis • Excellent • Little recurrence potential • When associated with Gardner’s syndrome. exostoses • Ossifying fibroma • Osteoblastoma • Focal sclerosing osteitis Treatment • Usually none • Local resection. malignant conversion of intestinal polyps is assured. . dense.280 PDQ ORAL DISEASE Osteoma Etiology • Sporadic form is idiopathic • May be a component of Gardner’s syndrome • Excludes maxillary and mandibular tori Clinical Presentation • Sporadic form with frontal and sphenoid sites predisposed • May be multiple • Solitary lesions rare in jaws Radiographic Findings • Well circumscribed.
Benign Nonodontogenic Tumors 281 .
• Anterior maxillary arch is favored site Diagnosis • Central islands or trabeculae of bone/cementum • Fibroblastic proliferation in a sheet-like configuration • Usually ulcerated with granulation tissue base Differential Diagnosis • Pyogenic granuloma • Peripheral giant cell granuloma • Peripheral fibroma • Peripheral odontogenic tumor • Osteosarcoma/chondrosarcoma • Metastatic neoplasm Treatment • Excision including underlying periosteum or associated periodontal ligament Prognosis • Recurrence occasionally seen. may rarely displace teeth • Usually in young adults and adolescents • Early lesions may bleed easily. commonly interdental • Nodular.282 PDQ ORAL DISEASE Peripheral Ossifying Fibroma Etiology • A reactive hyperplasia of the gingiva. may be related to chronic irritation • Periodontal ligament/membrane origin postulated Clinical Presentation • Exclusive gingival location. believed to be related to incomplete excision . sessile to pedunculated. usually ulcerated mass • Slow growing.
Benign Nonodontogenic Tumors 283 .
lips. adrenaline . and neck • Overlying skin and oral mucosa appear noninflamed • Mucosa may become secondarily erythematous. vesicular • Usually short-lived (24– 48 hours) Diagnosis • Nonspecific histology • Correlation of history and clinical findings Differential Diagnosis • Trauma (physical. shellfish. corticosteroids. nuts. medications) • Mechanism associated with immunoglobulin E (IgE)-mediated mast cell degranulation with subsequent histamine release • Drug reactions resulting in release of inflammatory mediators (bradykinin) • Some cases have a genetic basis: C1 esterase inhibitor deficiency or inhibitor dysfunction (autosomal recessive) • May be correlated with disease states characterized by the presence of circulating immune complexes Clinical Presentation • Soft. ulcerative.284 PDQ ORAL DISEASE Inflammatory Diseases Angioedema Etiology • Usually triggered by ingested antigens (eg. diffuse. fruits. painless swelling of face. or. rarely. cold) • Cellulitis • Vascular malformation • Acute contact stomatitis • Melkersson-Rosenthal syndrome (early stages) • Orofacial granulomatosis (early stages) Treatment • Elimination of possible etiologic/precipitating factor(s) • Antihistamines.
Inflammatory Diseases 285 Prognosis • Good to excellent .
or palate. and chronic lip enlargement • May be an incompletely expressed or oligosymptomatic form of Melkersson-Rosenthal syndrome Clinical Presentation • One or both lips may be diffusely enlarged and nontender. • May be associated with Crohn’s disease. • Lip swelling may herald similar changes of the gingiva. • Episodic swelling initially. contact sensitivity. superficial labial exfoliation or surface weeping/crusting may be noted.286 PDQ ORAL DISEASE Cheilitis Granulomatosa Etiology • Isolated. buccal mucosa. with progression to a persistent enlargement • Less often. sarcoidosis. idiopathic. dental abscesses Microscopic Findings • Demonstrates noncaseating epithelioid granulomas • Absence of organisms Diagnosis • History of intermittent to persistent asymptomatic lip swelling • Characteristic appearance • Lip or soft tissue biopsy (involved gingiva) • Rule out sarcoidosis (chest radiograph. serum angiotensinconverting enzyme levels) • Patch testing for contact allergens • Dental radiographs to rule out asymptomatic periapical pathology Differential Diagnosis • Angioedema • Cellulitis/erysipeloid reaction • Sarcoidosis • Crohn’s disease • Melkersson-Rosenthal syndrome • Cheilitis glandularis • Contact stomatitis .
• Clofazimine 100 mg daily for 60 days with reduction to a maintenance dose of 30 mg on alternate days • Metronidazole may also be effective at 250 mg three times daily for 1 month. psychological effects . • Dapsone may be effective (as per dermatitis herpetiformis dosing) • Surgical reduction (cheiloplasty) may be necessary. ophthalmologic involvement. Prognosis • Guarded • Must remain aware of possible neurologic manifestations.Inflammatory Diseases 287 Treatment • Local intralesional triamcinolone injections under local anesthesia • 5 to 10 mg total dose in depot fashion every 3 to 4 weeks to achieve response • Local treatment may be coupled with an initial systemic course of glucocorticoids. This may be coupled with intralesional corticosteroid placement.
288 PDQ ORAL DISEASE Drug-Induced Stomatitis (Stomatitis Medicamentosa) Etiology • Oral changes found in approximately 5% of those with cutaneous reaction to drugs • Mucosal alterations may result from the following: • Myelosuppression • Direct cytotoxic or cytostatic effect(s) on dividing epithelial cells • Xerostomic effects • Alterations of oral microbial flora Clinical Presentation • Painful. or ulcerative lesions • Nonkeratinized locations often affected initially • Fixed form of drug-associated eruptions relatively uncommon intraorally • Pseudomembranous necrotic surface may be noted Diagnosis • History • Clinical appearance Differential Diagnosis • Chemical or thermal burn • Erosive lichen planus • Pemphigus vulgaris • Mucous membrane (cicatricial) pemphigoid • Erythema multiforme • Acute herpetic gingivostomatitis • Candidiasis Treatment • Identification and withdrawal of offending drug • Symptomatic management including topical preparations (see “Therapeutics” section) . erythematous. erosive.
Inflammatory Diseases 289 • Systemic corticosteroids if mucosal reaction is not related to antineoplastic treatment Prognosis • Generally excellent .
mandibular. producing a reduplication of the cortex (“onion skin” effect).290 PDQ ORAL DISEASE Garré’s Osteomyelitis Etiology • Chronic. unilateral. dentoalveolar infection • Resultant bony inflammation extends to the periosteum. low-grade. usually first permanent molar • Radiographic features • Biopsy results showing periosteal osteoblastic reaction. Clinical Presentation • Usually an asymptomatic. minimally inflamed fibrous marrow Differential Diagnosis • Ewing’s sarcoma • Langerhans cell disease (histiocytosis X) • Osteosarcoma • Fibro-osseous lesion • Metastatic disease Treatment • Elimination of the infected focus (carious tooth to be extracted or filled) • Antibiotic administration early in treatment phase Prognosis • Good . bony hard asymmetry • Limited to children and young adults Radiographic Findings • Medullary mottling with (lucent and opaque) ill-defined margins • Periosteal-cortical expansion • Occlusal radiograph shows concentric or parallel layering of cortex Diagnosis • Carious mandibular tooth.
Inflammatory Diseases 291 .
• Rarely. blunted. some forms are associated with contact allergy (“plasma cell gingivitis”). • Fusospirochetal gingivitis plus poor oral hygiene and poor nutrition are associated with acute necrotizing ulcerative gingivitis. as follows: • Plaque associated: marginal inflammation to more generalized erythema and blunting of interdental papillae with rolled margins • Hormonally related: diffuse erythema and hyperplasia • Fusospirochetal: necrotic. such as those in pregnancy (pregnancy gingivitis). • Some are modified by hormonal changes. ulcerated interdental papillae with spontaneous bleeding.292 PDQ ORAL DISEASE Gingivitis Etiology • Variable • Most are microbiologic or plaque associated (simple marginal gingivitis). Clinical Presentation • Dependent on etiology. granular to velvety surface alteration Diagnosis • Identification of cause • Patch testing for contact allergens Differential Diagnosis • Acquired immunodeficiency syndrome–associated periodontal disease • Oral lichen planus • Mucous membrane (cicatricial) pemphigoid • Acute herpetic gingivostomatitis • Pemphigus vulgaris . foul odor • Allergy based: hyperplastic and bright red.
Inflammatory Diseases 293 Treatment • Local débridement and chlorhexidine rinses in cases of bacterial origin • Reduction of hormonal dosage • Elimination of allergen Prognosis • Excellent .
atrophic or hyperplastic epithelium • Candidal colonization of surface • Heavy. asymptomatic erythematous patch on dorsum of tongue • Paramedian erythema.294 PDQ ORAL DISEASE Median Rhomboid Glossitis Etiology • A benign. • Rarely may be hyperkeratotic • May be mistaken for a benign or malignant tumor Microscopic Findings • Papillary. inflammatory condition • Often related to yeast colonization (erythematous candidiasis) • Inflammatory process noted in response to overlying Candida population • Exact mechanism is unclear Clinical Presentation • Well-defined. location Treatment • Topical and/or brief course of systemic antifungal therapy (optional) • Observation Prognosis • Excellent . chronic inflammatory infiltrate Diagnosis • Clinical appearance. usually with focal atrophy of filiform papillae • Chronic forms may become multinodular.
Inflammatory Diseases 295 .
patchy radiolucency (“moth eaten”) Diagnosis • Presentation and radiographic findings • Microscopic evidence of intrabony inflammation. nonviable bone Differential Diagnosis • Osteosarcoma • Local extension of malignant tumor • Metastatic tumor • Osteoradionecrosis Treatment • Drainage and antibiotics for acute disease • Débridement. lymphadenitis • Sequestrum formation • Lower lip paresthesia. fever. osteoclastic resorption. sequestrectomy. • Most common organisms include staphylococci and streptococci Clinical Presentation • Pain. occasionally with acute disease in mandible • Associated soft tissue swelling Radiographic Findings • Acute phase may be unremarkable • Ill-defined. swelling.296 PDQ ORAL DISEASE Osteomyelitis Etiology • An acute or chronic inflammatory process within the medullary space or along the cortical surface of bone • Usually due to extension of a periapical abscess • Other common causes include physical trauma (fracture) or bacteremia. antibiotics for chronic disease • Reconstruction if necessary after disease is resolved Prognosis • Good . reduced osteoblastic activity. marrow fibrosis.
Inflammatory Diseases 297 .
débridement of bone preceded and followed by hyperbaric oxygen therapy • If necessary. usually > 60 Gy (6. • Minor damage to the irradiated bone produces a nonhealing wound. which. forming dead bone—necrosis.000 rads) • Radiation produces damage to the microvasculature. in turn. Differential Diagnosis • Metastatic tumor • Locally recurrent tumor • Osteomyelitis • Osteosarcoma • Radiation-induced sarcoma Treatment • After biopsy. Clinical Presentation • Usually affects the mandible • Bone pain • Exposed necrotic bone within radiation portal • External fistula formation • Pathologic fracture Radiographic Findings • Irregular zones of mixed radiopacity and radiolucency • Separation of nonvital bone (sequestrum) from remaining viable bone Diagnosis • Radiographic and clinical features • Biopsy results show nonvital bone. permitting a hypoxic state. leads to a hypocellular bony environment. resection and reconstruction .298 PDQ ORAL DISEASE Osteoradionecrosis Etiology • A serious complication of tumoricidal doses of radiation to the head and neck.
Inflammatory Diseases 299 • Necessary tooth extraction and elimination of focal infection within radiation portal 21 days prior to treatment • Excellent preventive dental care Prognosis • Guarded .
• Tenderness at root apex on palpation • Pain on biting or percussion of tooth Radiographic Findings • Radiolucency at apex of tooth • Size ranges up to 1 to 2 cm in diameter • Root resorption not uncommon Diagnosis • Radiographic features • Demonstration of nonvital pulpal component Differential Diagnosis • Periapical cemental dysplasia • Periapical cyst Treatment • Conventional endodontic therapy • Apical curettage/root end amputation if above measures fail • Extraction of involved tooth Prognosis • Excellent . pain and sensitivity develop.300 PDQ ORAL DISEASE Periapical Granuloma Etiology • A mass of inflamed granulation tissue • Forms secondary to pulp necrosis of the associated tooth • May develop following periapical abscess formation or may form as pulpal death eventuates without abscess precursor Clinical Presentation • Usually asymptomatic • With acute exacerbation.
Inflammatory Diseases 301 .
Differential Diagnosis • Tuberculosis • Lymphoma (non-Hodgkin’s. fever. cranial nerve palsies). • Over 90% of cases have abnormal chest radiograph. submandibular. Diagnosis • Demonstration of sarcoidal (noncaseating epitheloid) granulomas in at least two organ systems • Elevated serum angiotensin-converting enzyme levels are usually present. endocrine glands. such as the following. Hodgkin’s) • Deep fungal infection • Crohn’s disease . • Erythematous. granulomatous disease process • May represent a systemic response to a single provoking agent. • Multiple organ systems. • Other causes of granulomatous inflammation must be ruled out. and lacrimal glands may be enlarged. mycobacteria has been suggested but not proven • Possible role of genetic factors coupled with disordered reactions to foreign antigens Clinical Presentation • Mucocutaneous • Red to brown nodules/plaques with erythema nodosum features • Minor salivary glands of the lips and palate may be involved. and the reticuloendothelial and musculoskeletal systems • Heerfordt’s syndrome may be related to sarcoidosis (uveitis. but also liver.302 PDQ ORAL DISEASE Sarcoidosis Etiology • Unknown. the heart. hyperplastic gingiva • Salivary/lacrimal • Parotid. may be involved: • Particularly the lung. parotid gland enlargement.
Inflammatory Diseases 303 Treatment • Corticosteroids. if symptoms demand • Severe or unresponsive cases: methotrexate • Cutaneous lesions only: hydroxychloroquine • Intralesional corticosteroids Prognosis • Generally good .
low-grade toothbrush injury • At occlusal and incisal surfaces. improper tooth-brushing techniques • Pathologic wear of teeth associated with abnormal habits or function or consumption of abrasive to coarse diets • The so-called toothbrush abrasion at the gingival margin may be related to abnormal incisal or occlusal forces producing abfraction injury to enamel at the cementoenamel junction Clinical Presentation • Causally related appearance includes the following: • Incisal/occlusal wear related to habit or abrasive diet or substance • Cervical wear of posterior teeth with chronic. abrasion-related injury. are visible in advanced cases. containing tertiary dentin. a generalized loss of crown height • At the cervical margin (cementoenamel junction). horizontal V-shaped to saucerized notches (abfraction injury) • With exposure of significant root surface. and pipes.304 PDQ ORAL DISEASE Tooth Abnormalities Abrasion Etiology • Excessive or abnormal wearing of teeth • Commonly associated with use of smokeless tobacco. habitual grinding. cigars. diffuse loss of cementum and dentin • Pulp canals. abrasive dentifrices. Diagnosis • Clinical appearance Differential Diagnosis • Amelogenesis imperfecta • Dentinogenesis imperfecta .
Tooth Abnormalities 305 Treatment • Restorative dental techniques • Correction of habits. occlusal force discrepancies Prognosis • Good .
enamel qualities. or hypocalcification • Enamel hardness varies depending upon type of defect: normal hardness in hypoplastic form but deficient amounts of enamel. soft enamel in the hypocalcified variant but normal amounts of enamel • Color ranges from normal (hypoplastic) to dark yellow-brown (hypocalcified) • Radiographic changes range from normal density (hypoplastic) to less dense (hypocalcified) • May be noted in association with taurodontism (coronally enlarged dental pulps) • X-linked form demonstrates random vertical bands of normal and hypoplastic enamel Diagnosis • Clinical and radiographic features • Family history (autosomal.000 of population Clinical Presentation • One of three basic alterations of enamel may be seen: hypoplasia.306 PDQ ORAL DISEASE Amelogenesis Imperfecta Etiology • Intrinsic enamel defect that affects all teeth of both dentitions • Results from defective amelogenin genes on X and Y chromosomes and also chromosome 4 (tuftelin gene) • At least 16 variants noted based upon inheritance pattern. and radiographic features • Frequency of 1:14. hypomaturation. X-linked forms) Treatment • Full-crown restorations for esthetics • Genetic counseling .000 to 1:16.
Tooth Abnormalities 307 .
incisal-occlusal. • Asymptomatic Diagnosis • Characteristic appearance • Generally proportional to age Treatment • Usually does not require specific management • Elective restoration of occlusal/incisal surfaces to prevent overclosure of jaws in function Prognosis • Excellent . and lingual • Abnormal occlusal-incisal relationship can predispose to accelerated rates of attrition Clinical Presentation • Primary and permanent dentitions can be affected. buccal.308 PDQ ORAL DISEASE Attrition Etiology • Defined as a physiologic wearing of teeth secondary to normal function/mastication • Can involve all surfaces of teeth including interproximal. • Flattened occlusal surfaces and reduction of incisal height • The loss of interproximal tooth surface (usually enamel only) leads to gradual dental arch shortening.
Tooth Abnormalities 309 .
including laxative abuse • Cause may be biologic (neurometabolic disturbance). painless parotid gland enlargement. and nutritional counseling . brittle hair and nails. Up to 20% of college-age women are affected. psychotherapy. thermal hypersensitivity of teeth • Specific patterns of enamel destruction (perimolysis) are noted along the palatal and occlusal aspects of maxillary teeth. Diagnosis • Recognition of oral signs • Coordination of oral signs with other findings including dermatologic signs: lanugo-like body hair. asteatotic skin. gingivitis. Clinical Presentation • Oral signs include erosion of teeth. hand or finger calluses (related to self-induced vomiting) Differential Diagnosis • Diet-induced enamel loss • Chronic gastric reflux disease Treatment • Combined aggressive medical management. increased caries rate. behavioral management. sparing the buccal and labial surfaces. • Mandibular teeth usually are affected less severely. xerostomia.2 million adolescent and young adult females are affected in the United States. psychological (societal pressure for extreme thinness). food intake management. or combined (biopsychosocial) • Nearly 1. males are considerably less affected.310 PDQ ORAL DISEASE Bulimia Etiology • A compulsive-eating disorder characterized by repeated episodes of binge eating followed by vomiting or another form of purging.
.Tooth Abnormalities 311 Prognosis • Fair to good • Mortality (estimates range from 1–15%) is divided equally between medical complications (electrolyte disturbance. acute renal failure. cardiac complications) and suicide.
permanent teeth of normal color with thistle-shaped pulp chambers. frequent pulp stones noted Diagnosis • Combined clinical and radiographic features • Normal clinical color of permanent teeth and periapical lesions help to distinguish from dentinogenesis imperfecta • Clinical crowns of primary teeth are amber and opalescent. no other organs affected Clinical Presentation • Premature tooth loss • All teeth affected • Two forms. • Absent root formation (type I) • Thistle-shaped pulp chambers and pulp stones (type II) Differential Diagnosis • Chemotherapy-/radiation therapy–induced root development alteration • Pulpal dysplasia Treatment • Teeth usually unsalvageable (type I) • Observation • Genetic counseling Prognosis • Guarded . obliterated pulp chambers. as follows: • More severe form (type I) characterized by “rootless teeth. multiple periapical radiolucencies (periapical granulomas/cysts) • Less severe form (type II) characterized by amber-colored primary teeth with susceptibility to wear.312 PDQ ORAL DISEASE Dentinal Dysplasia Etiology • An inherited disorder (autosomal dominant) of circumpulpal dentin with associated alterations of root morphology.” with normal-colored crowns.
Tooth Abnormalities 313 .
roots are slender to spiked with pronounced cervical constriction and obliterative pulpal calcification • Constricted tooth cervix gives molar crowns a “tulip” profile Diagnosis • Clinical and radiographic appearance • Family history Differential Diagnosis • Osteogenesis imperfecta Treatment • Functional and esthetic restorations (full crowns) • Genetic counseling . Clinical Presentation • Primary and permanent dentition exhibit gray to brownish opalescence • Normal enamel fractures easily from defective underlying dentin • Severe tooth abrasion related to exposed dentin following enamel loss • Radiographically.314 PDQ ORAL DISEASE Dentinogenesis Imperfecta Etiology • Hereditary disorder (autosomal dominant) of dentin (1:8.000 frequency in population) • May be seen in association with osteogenesis imperfecta • Altered dentin matrix is related to the defective degradation of dentin phosphoprotein during dentinogenesis.
Tooth Abnormalities 315 .
• Smooth to polished appearance of maxillary incisors in chronic. less commonly. habits. underlying eating disorder.316 PDQ ORAL DISEASE Erosion Etiology • Acid dissolution of enamel and dentin • Loss of enamel and. amalgam fillings) and any protected enamel may be above the surrounding dentin. dentin secondary to chemical (usually acids) action/demineralization • Intrinsic sources relate to stomach acid presence within the oral cavity. occupation related) • Cupped dentin noted to occur more rapidly than adjacent enamel loss on occlusal surfaces • Existing metallic restorations (inlays. or chronic acidic reflux Differential Diagnosis • Amelogenesis imperfecta • Factitial injury Treatment • Identification and elimination of cause • Treatment of underlying etiology . sucking on lemons) • Chronic regurgitation/gastroesophageal reflux • Bulimia-related vomiting Clinical Presentation • Loss of enamel initially along lingual surfaces of anterior teeth (bulimia. creating a “ledge” effect. environmental exposure. high-volume consumers of beverages (phosphoric or citric acid–containing) Diagnosis • Correlation of appearance with diet. reflux) • Labial enamel loss (beverage related. • May be due to the following: • Occupational exposure to acids • Diet with acid exposure (phosphoric acid– containing beverages.
Tooth Abnormalities 317 • Dental restorative treatment subsequent to complete functional evaluation. vertical dimension. and esthetics Prognosis • Excellent .
Differential Diagnosis • Amelogenesis imperfecta • Tetracycline-associated staining Treatment • Restorative dental treatment • Cosmetic bleaching Prognosis • Excellent .318 PDQ ORAL DISEASE Fluorosis: Chronic Endemic Etiology • Excessive dietary levels of fluoride: greater than one part per million in drinking water (can lead to fluorosis in a dosedependent relationship) • Childhood ingestion of fluoride dentifrice on a chronic basis • Tooth enamel hypomaturation resulting from prolonged ingestion of abnormally high levels of fluoride during tooth development. Diagnosis • Characteristic appearance and distribution • Data concerning fluoride concentration in drinking water should be obtained. usually between 2 and 3 years of age Clinical Presentation • Enamel alterations ranging from local pitting to white opacity or deeper brown mottling • Distribution is symmetric and bilateral and occurs in all quadrants of the jaws.
Tooth Abnormalities 319 .
removal and replacement Prognosis • Not applicable .320 PDQ ORAL DISEASE Fusion Etiology • Merging of two tooth germs to create a single tooth Clinical Presentation • A single large tooth (macrodont) is noted. Radiographic Findings • Common or separate pulp canals and roots Diagnosis • Radiographic evaluation • One less tooth present in dental arch Treatment • If esthetics demand. • One less tooth will be present in the dental arch.
Tooth Abnormalities 321 .
322 PDQ ORAL DISEASE Natal Teeth Etiology • Usually indicates prematurely erupted deciduous teeth Clinical Presentation • Erupted teeth at birth • Almost always are incisors • 85% appear in mandible Treatment • If mobile. extraction • Possible retention for functional. esthetic reasons .
Tooth Abnormalities 323 .
numbness. t(7.324 PDQ ORAL DISEASE Malignant Nonodontogenic Tumors Ewing’s Sarcoma Etiology • Unknown • Chromosomal translocations t(11. and swelling often early complaints • Diffuse. lytic bone lesion • Cortical expansion variable • Second most common bone tumor of children/adolescents • Soft tissues of head and neck account for 11% of extraskeletal sites Diagnosis • Radiographs often show “moth-eaten” appearance and laminar periosteal bone reaction • Cortex may be eroded or expanded Differential Diagnosis • Osteosarcoma • Lymphoma • Peripheral neuroectodermal tumor of bone • Primitive rhabdomyosarcoma • Neuroectodermal tumor of infancy . irregular.q12) Clinical Presentation • 60% in males.22).22).q12) and expression of the MIC2 gene • Genetically related to primitive peripheral neuroectodermal tumor via translocations t(11. that is. t(7. over 95% in those under 20 years of age • Chiefly in bone and soft tissues • Highly malignant • Pain. (q24.21) noted • Gene rearrangement often noted. (22.22).
Malignant Nonodontogenic Tumors 325 Treatment • Radiation and multiagent chemotherapy Prognosis • 54 to 74% 5-year survival rate in localized osseous form • Late relapse not uncommon .
breast. kidney) • Accounts for < 1% of oral malignancies Clinical Presentation • Usually manifests in the jaws with pain and swelling • Not uncommon is loosening of teeth or pathologic jaw fracture • Soft tissue location is rare. stomach • Intraosseous lesions with lytic. lung. prostate. breast.326 PDQ ORAL DISEASE Metastatic Cancer Etiology • Spread of a primary malignancy to the oral cavity structures or jaws (usually from lung. • Most frequent sites of primary neoplasms are kidney. Diagnosis • Radiographic findings • Biopsy Differential Diagnosis • Primary soft tissue tumor • Primary osseous tumor • Periodontitis (localized) • Osteoradionecrosis Treatment • Local radiation • Combination chemoradiotherapy Prognosis • Poor . colon. colon. prostate. ill-defined radiolucencies Microscopic Findings • As with the primary tumor • Tumor marker studies (immunohistochemical) may be necessary to define the site of origin.
Malignant Nonodontogenic Tumors 327 .
MOM2. trismus. c-JUN. “moth-eaten” destruction • Cortical destruction • Soft tissue extension • Erosion of mandibular canal • 25% of cases have “sunburst effect” (radiating radiopaque spicules) Microscopic Findings • Sarcomatous stroma • Osteoid production by neoplastic cells • Four basic patterns (no prognostic significance) are as follows: • Osteoblastic • Fibroblastic • Chondroblastic • Telangiectatic . c-myc. CDK4. nasal or paranasal sinus obstruction • May masquerade as an odontogenic infection • Intraoral signs are as follows: • Tooth mobility (vertical) • Periapical radiolucency (teeth vital) • Distal displacement of terminal molar • Jaw mass may be ulcerated.5%) • Mutation/amplification of p53. Radiographic Findings • Early intraoral findings • Displacement of teeth • Root resorption • Absent or attenuated lamina dura • Uniformly widened periodontal membrane space • Later jaw bone findings • Lytic. c-fos. SAS Clinical Presentation • May present with pain paresthesia.328 PDQ ORAL DISEASE Osteosarcoma Etiology • May be associated with pre-existing bone disease such as the following: • Paget’s disease (10 to 15%) • Fibrous dysplasia (0.
radiographic. .Malignant Nonodontogenic Tumors 329 Diagnosis • Correlation of clinical. pathologic findings Differential Diagnosis • Fibro-osseous lesion • Osteomyelitis • Osteoradionecrosis • Metastatic tumor • Other form of sarcoma Treatment • Radical ablative surgery • Hemimandibulectomy • Partial maxillectomy ± orbital exenteration • Adjuvant chemotherapy/radiotherapy Prognosis • Survival ranges from 12 to 58% at 5 years • Mandibular lesions are associated with a greater survival rate than are maxillary lesions.
transplantation may be necessary. secondary to systemic disease. • The secondary form may be subtle. digitalis. Diagnosis • Appearance of tongue • Systemic complaints • Biopsy results: demonstration of amyloid deposits in tissues (tongue. • Generally symptom related (dialysis. . depending upon organ involvement) Prognosis • When renal impairment exists. gingival tissues may contain deposits of amyloid. or nodular submucosal alterations. gingiva) Differential Diagnosis • Hyalinosis cutis et mucosae (lipoid proteinosis) • Leukemic infiltrate • Lymphangioma • Neurofibromatosis • Hemodialysis-related disorder Treatment • Directed to underlying cause (secondary) • Localized amyloid tumors may be excised.330 PDQ ORAL DISEASE Metabolic and Genetic Disorders Amyloidosis Etiology • May be primary (idiopathic). or familial • Formation of a fibrillar protein deposited in soft tissues and visceral organs with associated levels of dysfunction Clinical Presentation • The primary form may produce obvious tongue enlargement (macroglossia) and associated purpura.
Metabolic and Genetic Disorders 331 .
Radiographic Findings • Symmetric.3 • No associated metabolic or biochemical alterations noted • Possible linkage/association with Noonan’s syndrome Clinical Presentation • Early signs in childhood • Bilateral.332 PDQ ORAL DISEASE Cherubism Etiology • Autosomal-dominant. expansile radiolucencies of mandibular body and ramus • Impacted/displaced teeth common • Thinned cortices with scalloped medullary margins • Older patients may exhibit maturation with bone fill in some areas but with preservation of expanded bony profile. fibroblast/giant cell–containing condition • May be secondary to somatic mutation. • Unerupted teeth often noted • Facial features include lower-third fullness and scleral exposure at a forward resting gaze. multiloculated. symmetric enlargement of mandible • Maxillary involvement less common and less prominent • Dental arch/occlusal discrepancies may be noted. Diagnosis • Clinical appearance • Radiographic findings Differential Diagnosis • Central giant cell granuloma (multiple) • Fibrous dysplasia • Langerhans cell disease (histiocytosis X) • Hyperparathyroidism • Multiple odontogenic keratocysts . mapping to chromosome 4p16.
but variably so . ranging from cosmetic recontouring to local curettage early in lesion development • Active surgical intervention should be deferred until after the pubertal growth spurt. if possible.Metabolic and Genetic Disorders 333 Treatment • Variable. Prognosis • Stability usually noted by end of skeletal growth • Often regresses into adulthood.
treatment options are as follows: • Early orthodontic intervention • Surgical exposure of unerupted teeth • Extraction of supernumerary teeth . high-arched quality • Delayed closure of mandibular symphysis • Multiple unerupted and malpositioned teeth with lack of cellular cementum • Multiple supernumerary teeth Diagnosis • Clinical features • Radiographic findings (skull.334 PDQ ORAL DISEASE Cleidocranial Dysplasia Etiology • Autosomal-dominant trait with high penetrance and variable expressivity • Mutations in SH3-binding protein on chromosome 4p16.3 • Widespread membranous and endochondral defects in craniofacial complex Clinical Presentation • Chief head and neck manifestations include the following: • Defective ossification • Wormian bones with calvarial defects • Delayed fontanelle and suture closure • Variably developed clavicles often a prominent skeletal finding • Long. chest) Differential Diagnosis • Achondroplasia • Pyknodysostosis • Hydrocephalus Treatment • Genetic counseling • For dental abnormalities. narrow neck with variably drooped shoulders • Midface deficiency secondary to hypoplasia of facial bones and paranasal sinuses • Ocular hypertelorism • Palate with narrow. jaw.
.Metabolic and Genetic Disorders 335 • Surgical correction of jaw deformities • Dental reconstruction Prognosis • Stability with growth cessation • Dental and oral rehabilitation can proceed as per usual after surgery (see above) is completed.
chief oral finding is well-defined. jaws) • Histologic findings: identical to central giant cell granuloma of jaws Differential Diagnosis • Cherubism • Renal disease (osteodystrophy) • Paget’s disease of bone (skull)—early stages • Multiple odontogenic keratocysts (nevoid basal cell carcinoma syndrome) Treatment • Primary hyperparathyroidism: removal of abnormal gland(s) • Secondary hyperparathyroidism: management of renal disease Prognosis • Good . psychotic-like state • Fibrous/lytic bone lesions.336 PDQ ORAL DISEASE Hyperparathyroidism Etiology • Primary form usually due to parathyroid adenoma • Secondary form related to altered renal vitamin D metabolism with secondary hypocalcemia • Excessive parathormone secretion common to all forms Clinical Presentation • Classic triad in patients over 60 years includes the following: • Renal calculi/nephrolithiasis • Subperiosteal resorption of phalanges • Lethargy. cyst-like radiolucencies of jaw(s) • Osteoporotic bony changes • Loss of lamina dura • Duodenal ulcer formation Diagnosis • Increased serum calcium levels (primary) • Increased urinary hydroxyproline levels • Elevated serum parathormone • Radiographic changes (phalanges.
Metabolic and Genetic Disorders 337 .
1 every 6 h × 2–3 d • Prednisone 10 mg tablets #12. which may include systemic immunosuppressive and/or anti-inflammatory drugs. Candidiasis • Identify and correct provocative factors. • Refer to a dermatologist. 1 tablet 5 times daily × 10 d • Fluids • Analgesia Acute Necrotizing Ulcerative Gingivitis • Débridement of necrotic tissue • Aggressive oral hygiene and plaque control • Metronidazole 250 mg #40. 1 every 6 h × 2–3 d • Doxepin 25 mg tablets #12. for ongoing care. 1 tablet twice daily × 10 d • Acyclovir 400 mg #50. or an ophthalmologist. 4 tablets daily × 3 d Aphthous Stomatitis • See “Recurrent Aphthous Stomatitis.000 units/mL).” Behçet’s Disease • Treat as for aphthosis (see “Recurrent Aphthous Stomatitis”). depending on organ involvement. rinse 5 mL and swallow 4 times/d • Clotrimazole (Lotrimin) solution 1%. • Topical therapy • Nystatin oral suspension (100. rinse 5 mL and swallow 4 times/d . 1 4 times daily × 10 d Angioedema • Systemic therapy • Antihistamine: diphenhydramine 50 mg capsules #12. a rheumatologist.338 PDQ ORAL DISEASE Therapeutics Actinomycosis • Systemic therapy: penicillin or tetracycline in large doses for 3–6 mo • Wide excision of infected tissue Acute Herpetic Gingivostomatitis • Systemic therapy • Valacyclovir 500 mg #20.
1 tablet every day with breakfast × 21 d • Itraconazole (Sporanox) 200 mg #21. 1 tablet every other day for days 8–21 • Ketoconazole (Nizoral) 200 mg #21. 8-8-6-6-4-42-2 mg-stop – Will shorten the course of an individual episode but not change the natural history of the disease • Dapsone 25 mg tablets – Check baseline complete blood count (CBC). inject 1–3 mL per session with sessions at 3–4 wk intervals • Systemic antibiotic: tetracycline 500 mg tid • Systemic corticosteroids: prednisone 5 mg tablets #40 – Take each morning for 8 d with breakfast. 8-8-6-6-4-42-2 mg. stop – Will shorten the course of an individual episode but not change the natural history of the disease Cheilitis Granulomatosa • Challenging to treat • Trials of therapy • Intralesional corticosteroids such as triamcinolone acetonide 5–10 mg/mL. dissolve 1 troche in mouth 5 times/d • Clotrimazole vaginal tablets 1/ 2 of 500 mg tablet dissolved in mouth bid • Systemic therapy • Fluconazole (Diflucan) 100 mg #15. inject 1–3 mL per session with sessions at 3–4 wk intervals • Systemic antibiotic: tetracycline 500 mg tid • Systemic corticosteroid: prednisone 5 mg tablets #40 – Take each morning for 8 with breakfast. 2 tablets on the first day. and glucose-6-phosphate red blood cell enzyme level before treatment. .Therapeutics 339 • Clotrimazole troches (Mycelex) 10 mg. 1 tablet every day with breakfast × 21 d • May use shorter duration for less severe infections Cheilitis Glandularis • Challenging to treat • Trials of therapy • Intralesional corticosteroids as triamcinolone acetonide 5–10 mg/mL. liver function tests. urinalysis. 1 tablet days 2–7.
viscous lidocaine 90 mL. • Option 2 – Dexamethasone 100 mg. 2/d × 4 d. and 5 daily thereafter – Check CBC and liver function every month for 3 mo. 4 × 7 d. inject 1–3 mL per session with sessions at 3–4 wk intervals • Systemic antibiotic: tetracycline 500 mg tid • Systemic corticosteroid: prednisone 5 mg tablets #80 – Take each morning with breakfast for 16 d as 8/d × 4 d. and glucose-6-phosphate red blood cell enzyme level before treatment. 6/d × 4 d. distilled water 180 mL – Swish 5 mL for 2 min and expectorate 3–4 times/d. 1 × 3 d. . 3 × 3 d. 4/d × 4 d. 2 × 3 d. stop – Will reduce disease activity as topical corticosteroids or systemic nonsteroidal anti-inflammatory drugs (NSAIDs) are started • Dapsone 25 mg tablets – Check baseline CBC. Maalox suspension to 275 mL – Swish 5 mL for 2 min and expectorate 3–4 times/d. – Take each morning with breakfast. diphen hydramine 200 mg. 3 × 3 d. 4 × 7 d. urinalysis. Maalox suspension 90 mL. – Use for long-term control of disease Crohn’s Disease • Challenging to treat • Trials of therapy • Intralesional corticosteroids such as triamcinolone acetonide 5–10 mg/mL. liver function tests.340 PDQ ORAL DISEASE – Take each morning with breakfast. 2 × 3 d. viscous lidocaine 60 mL. sorbitol 15 mL. and 5 daily thereafter – Check CBC and liver function every month for 3 mo. then every 3 mo thereafter. – Use for long-term control of disease Drug-Induced Stomatitis (Stomatitis Medicamentosa) • Topical therapy (compounded rinses) • Option 1 – Diphenhydramine 200 mg. 1 × 3 d. then every 3 mo thereafter.
viscous lidocaine 90 mL. distilled water 180 mL – Swish 5 mL for 2 min and expectorate 3–4 times/d. • Systemic therapy • Prednisone 5 mg tablets #80 – Take each morning with breakfast for 16 d as 8/d × 4 d. Geographic Tongue • Brush tongue surface 10–15 times with dentifrice after meals and at bedtime to remove debris that causes halitosis. 1 tablet every 4 h for 7 d or 1 tablet bid-tid as prophylaxis Exfoliative Cheilitis • Identify possible topical or drug-related causative agents (eg. 4/d × 4 d. stop – Will reduce disease activity as topical corticosteroids or systemic NSAIDs are started • Acyclovir 200 mg tablets #42 (if triggered by herpes simplex virus infection). 6/d × 4 d. diphenhydramine 200 mg. mouthwash. stop • Will reduce disease activity as topical corticosteroids or systemic NSAIDs are started Erythema Multiforme • Topical therapy (compounded rinses) • Option 1 – Diphenhydramine 200 mg. • Topical therapy: see “Candidiasis” • Systemic therapy: see “Candidiasis” Fissured Tongue • Brush tongue surface 10–15 times with dentifrice after meals and at bedtime to remove debris that causes halitosis.Therapeutics 341 • Systemic therapy: prednisone 5 mg tablets #80 • Take each morning with breakfast for 16 d as 8/d × 4 d. 2/d × 4 d. 4/d × 4 d. 2/d × 4 d. 6/d × 4 d. toothpaste. . gold. Maalox suspension 90 mL. lipstick). sorbitol 15 mL. • Option 2 – Dexamethasone 100 mg. viscous lidocaine 60 mL. • Determine if factitial cause(s) is present. Maalox suspension to 275 mL – Swish 5 mL for 2 min and expectorate 3–4 times/d.
342 PDQ ORAL DISEASE • Topical therapy • Fluocinonide gel/cream 0. dissolve 1 troche in mouth 5 times/d • Clotrimazole vaginal tablets 1/ 2 of 500 mg tablet dissolved in mouth bid • Tacrolimus (Protopic) ointment 0. 1 tablet 4 times daily × 10 d • Dicloxacillin 250 mg tablets #40.1% 60 g. 1 tablet 4 times daily × 10 d . • Topical therapy: dilute H2O2 (1 part 3% H2O2:1 part H2O). apply after meals and at bedtime • Clotrimazole troches (Mycelex) 10 mg. apply after meals and at bedtime Hairy Tongue • Brush tongue surface 10–15 times with dentifrice after meals and at bedtime to remove debris that causes halitosis.05% 60 g. brush tongue after meals and at bedtime for black hairy tongue Hand-Foot-and-Mouth Disease • Fluids • Analgesia • Recovery expected quickly Herpangina • Fluids • Analgesia • Recovery expected quickly Herpes Zoster • Topical therapy • Calamine lotion for wet. 2 tablets 5 times daily × 7–10 d • Famciclovir 500 mg tablets #21. 1 tablet 4 times daily × 10 d • Erythromycin base 250 mg tablets #40. 2 tablets 3 times daily × 7 d Impetigo • Topical therapy: mupirocin ointment applied twice daily • Systemic therapy • Penicillin V potassium 250 mg tablets #40. 1 tablet 3 times daily × 7 d • Valacyclovir 500 mg tablets #42. oozing cutaneous lesions • Doxepin (Zonalon) cream for pain relief of acute lesions • Systemic therapy • Acyclovir 400 mg tablets #100.
apply after meals 3 times daily. 6/d × 4 d.Therapeutics 343 Lichen Planus • Topical therapy • Betamethasone cream (0.05% 60 g. repeat every 6 mo to monitor for retinal toxicity Lupus Erythematosus • Topical therapy • Fluocinonide gel/cream 0. • Hydroxychloroquine (Plaquenil) 250 mg #100. 2 × 3 d. and 5 × daily thereafter – Check CBC and liver function every month for 3 mos. apply after meals and at bedtime • Tacrolimus (Protopic) ointment 0.1%) 60 g. 2/d × 4 d. urinalysis. do not eat or drink for 30 min. – Use for long-term control of disease. 2 tablets with breakfast for 4 wk. liver function tests.05% 60 g. 3 × 3 d. do not eat or drink for 30 min • Intralesional therapy: triamcinolone acetonide 5–10 mg/mL. taper frequency depending on response • Intralesional therapy: triamcinolone acetonide 5–10 mg/mL.1% 30 g. 4 × 7 d. apply after meals and at bedtime • Tacrolimus (Protopic) ointment 0. apply after meals and at bedtime • Fluocinonide gel/cream 0. stop – Will reduce disease activity as topical corticosteroids or systemic NSAIDs are started • Dapsone 25 mg tablets – Check baseline CBC. 1 × 3 d. 4/d × 4 d. inject 1–3 mL per session with sessions at 3–4 wk intervals . apply after meals 3 times dailyand at bedtime. and glucose-6-phosphate dehydrogenase enzyme level before treatment.1% 30 g. then every 3 mo thereafter. inject 1–3 mL per session with sessions at 3–4 wk intervals • Systemic therapy • Prednisone 5 mg tablets #80 – Take each morning with breakfast for 16 d as 8/d × 4 d. – Take each morning with breakfast. then 1 tablet daily for maintenance – Baseline ophthalmology consultation.
urinalysis and glucose-6-phosphate dehydrogenase enzyme level before treatment. depending on organ involvement. • Do not apply to ulcers. apply topical therapy: fluocinonide 0. 1 × 3 d. Pemphigoid • Refer to a dermatologist or an ophthalmologist. 4 × 7 d. • May be used for 1–2 h with mouthguard for occlusive therapy • Systemic therapy for severe.344 PDQ ORAL DISEASE Melkersson-Rosenthal Syndrome • See “Fissured Tongue. . 3 × 3 d. 2/d × 4 d. • For localized oral pemphigoid/gingival pemphigoid.” • Orofacial granulomatosis—see “Cheilitis Granulomatosa” Nevus • All pigmented nevi should be excised. which may include systemic immunosuppressive and/or anti-inflammatory drugs. – Take each morning with breakfast.05% gel/cream 60 g • Apply to early lesions after meals and at bedtime. 2 × 3 d. stop – Will reduce disease activity as topical corticosteroids or systemic NSAIDs are started • Dapsone 25 mg tablets – Check baseline CBC. then every 3 mo thereafter. 4/d × 4 d. if reasonable from a surgical point of view. – Use for long-term control of disease • Tetracycline and niacinamide – 500 mg of each administered tid – Use for long-term control of disease Pemphigus Vulgaris • Coordinate overall management with patient’s internist/primary care physician since treatment of this disease requires systemic immunosuppression and/or use of anti-inflammatory drugs. chronic disease • Prednisone 5 mg tablets #80 – Take each morning with breakfast for 16 d as 8/d × 4 d. liver function tests. for ongoing care. and 5 × daily thereafter – Check CBC and liver function every month for 3 mo. 6/d × 4 d. • Management of oral lesions will consist of systemic immunosuppressive agents.
apply after meals and at bedtime • Systemic therapy: griseofulvin 250 mg tablets #150. • Management of prednisone side effects is important. • Systemic therapy: prednisone 10 mg tablets #150 • Take each morning with breakfast at a total daily dose of 1 mg/kg of body weight. dosing spaced morning and evening • Mycophenolate mofetil 500 mg tablets.” • Systemic therapy: analgesics prn . • Corticosteroid-sparing systemic therapy • Azathioprine 1–3 mg/kg. take 1 with each meal for 7 wk Pyostomatitis Vegetans • Seek the underlying inflammatory bowel disease. – Continue on orally administered immunosuppressants. 5 mL rinsed bid • Chlorhexidine 0. – 15–30 mL rinsed bid • See “Drug-Induced Stomatitis. • Topical therapy: fluocinonide gel/cream 0. • Taper slowly over several months as clinical response permits to maintenance dosing.5 g bid • Severe or unresponsive disease • Plasmapheresis • Pulse cyclophosphamide (Cytoxan) IV for 3 wk – Monitor response. 1.12% compounded as alcohol-free formula – Store in a light-protective container. • See “Crohn’s Disease.” Radiation-Induced Mucositis • Topical therapy • Benzydamine rinses • Saline/bicarbonate rinses 2.Therapeutics 345 • Local/intralesional therapy may be a useful adjunct following an initial good measurable response to systemic glucocorticosteroid dosing.5 mL each in 125 mL water.05% 60 g. • IVIg therapy • Local therapy for focal residual lesions: intralesional triamcinolone suspension 10 mg/mL Plasma Cell Gingivitis • Identify contact allergen(s) and avoid exposure.
urinalysis and glucose-6-phosphate dehydrogenase enzyme level before treatment. apply to ulcers after meals and at bedtime • Fluocinonide 0. distilled water 180 mL Rinse 5 mL—expectorate 4–6 times daily. if tolerated. diphenhydramine 200 mg.5 mg/5 mL nonalcoholic elixer) 200 mg.05% gel/cream 60 g – Apply to early lesions after meals and at bedtime.5 mg tablets – Take 1 each morning with breakfast for 1 wk. painful. • Complex aphthosis • Laboratory evaluation for “correctable causes”: CBC. 1 tablet 3 times/d with meals – Dapsone 25 mg tablets – Check baseline CBC. red blood cell folate. viscous lidocaine 90 mL. increase to 2 tablets each morning – May suppress disease activity – Pentoxifylline (Trental) 400 mg tablets. • Compounded rinse option 2 Dexamethasone (10 mg/mL) 10 mL. Maalox suspension 85 to 275 mL Rinse 5 mL—expectorate 3–5 times daily. viscous lidocaine 60 mL. – Do not apply to ulcers. Maalox suspension 90 mL. serum iron studies. stop – Will shorten the course of an individual episode but not change the natural history of the disease – Colchicine 0. liver function tests. serum vitamin B12.346 PDQ ORAL DISEASE Recurrent Aphthous Stomatitis (Aphthosis) • Classify disease into simple versus complex • Simple aphthosis • Amlexanox paste 5 g (Aphthasol). • Compounded rinse option 1 – Diphenhydramine parenteral (or 12. chronic complex aphthosis – Prednisone 5 mg tablets #40 – Take each morning with breakfast for 8 d 8-8-6-6-4-42-2 mg. . serum ferritin. serum zinc • Topical therapy as for simple aphthosis • Systemic therapy for severe.
tablet. apply at the onset of symptoms every 2 h × 4 d • Docosanol cream (Abreva) 10%.5 g tube. – Use for long-term control of disease. 1 × 3 d. • Drink milk with meals • Saliva substitutes • Liquid. Recurrent Herpes Simplex Labialis or Stomatitis • Topical therapy • Penciclovir cream (Denavir) 1% 1. • Use Vaseline on lips at night (a thin coating). apply topically at the onset of symptoms q2–3h 5 times daily • Acyclovir ointment 5% 3 g tube. then every 3 mo thereafter. take 1 capsule 3 times daily . • Avoid alcohol-containing mouth rinses. • Limit caffeine intake. • Avoid drugs that produce xerostomia.Therapeutics 347 – Take each morning with breakfast. or gel forms • Available over the counter • Systemic therapy • Pilocarpine (Salagen) 5 mg tablets #100. 2 × 3 d. 3 × 3 d. take 1 tablet 3 times daily • Cevimeline capsules (Evoxac) 30 mg capsules #100. • Acyclovir 200 mg tablets – 3 tablets daily to prevent reactivation in bone marrow transplant recipients Sjögren’s Syndrome • Topical therapy • Moisten mouth with cool water or ice chips. apply at the onset of symptoms 6 times daily × 7 d • Systemic therapy • Acyclovir 200 mg tablets #35 – 1 tablet 5 times daily × 7 d – Start medication with premonitory symptoms to shorten the course of the episode. and 5 × daily thereafter – Check CBC and liver function every month for 3 mo. 4 × 7 d.
sorbitol 15 mL. Maalox suspension 90 mL.5 mg/kg for first 2 mo Wegener’s Granulomatosis • Systemic therapy • Sulfamethoxazole/trimethoprim (Bactrim DS) Septra DS 1 twice daily • Prednisone 1 mg/kg daily • Cyclophosphamide Zoster • See “Herpes Zoster. distilled water 180 mL – Swish 5 mL for 2 min and expectorate 3–4 times/d • Option 2 – Dexamethasone 100 mg. Maalox suspension to 275 mL – Swish 5 mL for 2 min and expectorate 3–4 times/d • Systemic therapy • Prednisone 5 mg tablets #80 – Take each morning with breakfast for 16 d as 8/d × 4 d. 6/d × 4 d.348 PDQ ORAL DISEASE Stevens-Johnson Syndrome • Topical therapy (compounded rinses) • Option 1 – Diphenhydramine 200 mg. viscous lidocaine 60 mL. 2/d × 2 d.” . 1 tablet every 4 h for 7 d or 1 tablet bid-tid as prophylaxis Tuberculosis • Systemic therapy (prolonged treatment with at least 2 drugs) • Isoniazid 300 mg daily × 6 mo • Rifampin 450–600 mg daily × 6 mo • Ethambutol 15 mg/kg daily for first 2 mo • Pyrazinamide 1. 4/d × 4 d. diphenhydramine 200 mg. stop – Will reduce disease activity as topical corticosteroids or systemic NSAIDs are started • Acyclovir 200 mg tablets #42 (if triggered by herpes simplex virus infection). viscous lidocaine 90 mL.5–2.
Redman RS. Curlin MU. Oral leukoplakia status six weeks after cessation of smokeless tobacco use.35:354–9.23:181–7. Dermatol Surg 1997. Williams DM. Axell T. Grbic JT. Fettig A. Silverman S Jr. McCreary CE. Ultrastruc Pathol 1999. Pogrel MA.90:723–30. AIDS Patient Care STDS 1997.23:15–21. Oral Dis 1999. A treatment review. Dufresne RG Jr. Eifler CW. International Collaborative Group on Oral White Lesions. Mirbod SM. Lamster IB. Topical corticosteroids in association with miconazole and chlorhexidine in the long-term management of atrophic-erosive oral lichen planus: a placebo-controlled and comparative study between clobetasol and fluocinonide. Candidiasis: pathogenesis.37:338–43. Carrozzo M. . Smith CJ. Br J Oral Maxillofac Surg 1999. J Calif Dent Assoc 2000. Oral manifestations of HIV infection. Carbone M. et al.11:18–24. Cruchley AT. Clinical management of oral lichen planus. Epstein-Barr virus. Oral Dis 1997. 1994. May 18–21.66:252–6. Ahing SI. Oral Oncol 1999. Houston GD. Proliferative verrucous leukoplakia and its related lesions. McCartan BE. and treatment. clinical characteristics.5:44–9. Tobacco-associated lesions of the oral cavity: Part I. et al. Oral white lesions with special reference to precancerous and tobacco-related lesions: conclusions of an international symposium held in Uppsala.349 Additional Reading White Lesions Appleton SS.3 Suppl 1:S156–63. Pindborg JJ.25:49–54. Young LS. Actinic cheilitis. Suarez P. Oral hairy leukoplakia: an ultrastructual study and review of the literature. Guccion JG.28:942–8. Proliferative verracous leukoplakia of the gingiva. J Oral Pathol Med 1996. van der Waal I. Batsakis JG. Martin GC. Sweden. Conrotto D. Brown JP. el-Naggar AK. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2000. Nonmalignant lesions. Niedobiek G.130:945–54. Biology and disease. J Can Dent Assoc 2000. J Am Dent Assoc 1999.
Oral Dis 1999. Concomitant leukoplakia in patients with oral squamous cell carcinoma. et al. Bacillary angiomatosis affecting the oral cavity. High malignant transformation rate of widespread multiple oral leukoplakias. Crighton AJ. Sciubba JJ. Rogers RS III. Sugiura C. Increased genetic damage in oral leukoplakia from high risk sites: potential impact on staging and clinical management. et al. Egorshin EV. Kaposi’s sarcoma-associated herpesvirus: a new DNA tumor virus. Annu Rev Med 2001. Bekic M.78:145–50. Oral Dis 2000. Mucous membrane plasmacytosis of the upper aerodigestive tract. Molecular defects in rare bleeding disorders: hereditary haemorrhagic telangiectasia. Semin Cutan Med Surg 1997. Walsh PM.5:206–9. Olsen KD. Thromb Haemost 1997. Lam WL. Smeele LE.29:91–6. Report of two and review. van der Meij EH.66:22–5. Weiss RA. Magee GJ.5:15–9. van der Waal I. Oral Dis 1999. Rugg EL. Am J Surg Pathol 1994. Samaranayake LP. Zhang I. Saito T. Wilson NJ.5:321–4. 6:85–91. J Oral Pathol Med 2000. A clinicopathologic study. Red/Blue Lesions Boshoff C. Cancer 2001. et al. Crit Rev Oral Biol Med 1995. Ferreiro JA. J Oral Pathol Med 1999. Femopase F. Oral leukoplakia. Chisholm DM. Allison WE.52:453–70. Boshoff C.16:328–36. Epstein JB. The oral effects of smokeless tobacco. A mutation in mucosal keratin K4 is associated with oral white sponge nevus. J Can Dent Assoc 2000. .356: 517–34. Mountain RE. Rugg EL.6:147–60.350 PDQ ORAL DISEASE Reichart PA. McLean WH. Hirai A. Plasma cell mucositis: a review and case report. Nat Genet 1995.28:183–6.91:2148–55. Philos Trans R Soc Lond B Biol Sci 2001. Oral Dis 1999. Schepman KP. Diseases of the lips. Smith ME. Pathology and clinical correlates in oral candidiasis and its variants: a review. Lopez de Blanc S. Shovlin CL. Cheung KJ Jr. et al.18:1048–53. Philipsen HP. Sambuelli R. Identification of two novel mutations in keratin 13 as the cause of white sponge naevus. Epidemiology and pathogenesis of Kaposi’s sarcomaassociated herpesvirus. et al.11:450–2. Chang Y.
10:585–9. The clinical and immunopathological manifestations of anti-epiligrin cicatricial pemphigoid. Egan CA. J Am Acad Dermatol 2001.354:667–72. Nousari HC. Scully C. New and emerging therapies for diseases of the oral cavity. Clin Microbiol Rev 2000. Carrozzo M.13:470–511. Marinkovich MP. Semin Cutan Med Surg 1997. Mycoplasma pneumoniae infection is associated with Stevens-Johnson syndrome. The clinical spectrum of desquamative gingivitis.43:571–91. Adv Dent Res 1996. Dermatol Clin 1997. Korman NJ. Molecular biological aspects of acquired bullous diseases. Gandolfo S. Liesegang TJ. Samonis G. Dermatol Clin 2000.15:341–9. . Dermatol Clin 2000. Mantadakis E. Dermatol Clin 1999. Autoimmune aspects of pemphigus vulgaris and mucosal pemphigoid. Pathogenesis of group A streptococcal infections. Engineer L. Yancey KB. Update on inherited bullous dermatoses. Fleming TE. J Am Acad Dermatol 2000. Herpesvirus-induced diseases: oral manifestations and current treatment options. Tay YK. Anhalt GJ. Weston WL. Eur J Dermatol 2000.7:1389–94.16:308–13. Emerging treatment for epidermolysis bullosa acquisita.18:113–25. Porter SR.88: 56–68. Sciubba JJ. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1999. Cunningham MW. Ahmed AR. Scully C. J Am Acad Dermatol 1996. Mayo Clin Proc 1999. Crit Rev Oral Biol Med 1998.10:52–6. Sadick NS.18:127–37.35(5 Pt 1):757–60.44:818–28. Lancet 1999. Orofacial viral infections in the immunocompromised host. Kerman NJ. et al. Current aspects of bacterial infections of the skin. New and emerging therapies in the treatment of blistering diseases. Pemphigus and bullous pemphigoid.17:473–85.28:911–21. Maraki S. J Calif Dent Assoc 2000.Additional Reading 351 Vesiculobullous Diseases Birek C. Oncol Rep 2000. Update on mucous membrane pemphigoid: a heterogeneous immune-mediated subepithelial blistering entity. Huff JC. Varicella zoster viral disease. not erythema multiforme (von Hebra). Cicatricial pemphigoid. Popovsky JL.9:162–78. a recently defined subepithelial autoimmune blistering disease. Dabelsteen E. Camisa C.74:983–98.
Current and potential therapies for the treatment of herpesvirus infections. Smokeless tobacco and oral cancer: an assessment of evidence derived from laboratory animals.23:35–46.38:89–101. Capone RB. J Nat Cancer Inst 2000. Evidence for causal association between human papilloma virus and a subset of head and neck cancers. Lee KF. Radiother Oncol 1996. Johnson NW.352 PDQ ORAL DISEASE Uitto J. Quintessence Int 1997. Molecular complexity of the cutaneous basement membrane zone. Semin Diagn Pathol 1996.92:709–20. Tuberculosis of the oral cavity: a case report. Risk factors for squamous cell carcinoma of the oral cavity in young people—a comprehensive literature review. Acquired skin disease of hemidesmosomes. De Aguiar MC. Pharyngitis. Cancer Res 1996. et al. Lingen M. Lee WI. Zillikens D. Warnakulasuriya KA. A genetic progression model for head and neck cancer: implications for field cancerization. et al. Oral Oncol 2001. Llewellyn CD.13:118–27. Adenitis). Callen JP. Ulcerative Conditions Bentzen SM. Ruifrok AC. Grasso P. Califano J. Koch WM. J Dermatol Sci 1999. The possible association between oral lichen planus and oral squamous cell carcinoma: a clini- . Mignogna MD.37:401–18. Aphthous stomatitis. Pulkkinen L.56:2488–92. Prog Drug Res 2001. Yang MH.16:323–7. Semin Cutan Med Surg 1997.56:77–120.28:745–7. Oral manifestations of collagen vascular disease. Repair capacity and kinetics for human mucosa and epithelial tumors in the head and neck: clinical data on the effect of changing the time interval between multiple fractions. Thames HD. Sturgis EM. Mato MJ. Granulomatous disorders of the oral mucosa. Clayman G. Gillison ML. Clin Rheumatol 1999.20:134–54. Mann AH. Curr Opin Oncol 2001.13:176–82. Eveson JW. Villarreal EC.36:1015–29. Favia G. Food Chem Toxicol 1998. van der Reit P.18: 207–13. Lo Muzio L. Mol Biol Rep 1996. Westra WH. de Araujo VC. et al. Arrais MJ. PFAPA syndrome (Periodic Fever. Squamous cell carcinoma of the head and neck in nonsmokers: clinical and biologic characteristics and implications for management. Kies MS.
de Almeida OP. Slootweg PJ. Prince S.91:622–35. Melanotic macule of the oral mucosa: a clinicopathologic study of 105 cases. Dermatol Clin 1996. Two cases of oral pigmentation associated with quinidine therapy. Semin Diagn Pathol 2001. Squamous carcinoma of the tongue: review. Oral Oncol 1998. Buchner A.18: 34–46.44:147–56. Sonis ST.127:1202–13.20:260–2. Sposto MR.14:371–9. Oral Surg Oral Med Oral Pathol 1979. . Woo SB. Johnstone BM. Yi ES.9:249–56. et al. Wegener’s granulomatosis. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1997.83:672–9. Hansen L. 48:244–9. 1982–1997. Oral Dis 1997. A review of the literature. et al. Oral Surg Oral Med Oral Pathol 1988. Bailey BM.Additional Reading 353 cal evaluation on 14 cases and review of the literature. Oral mucosal melanomas: the WESTOP Banff workshop proceedings. Bothwell M. Tralongo V. Amalgam pigmentation (amalgam tattoo) of the oral mucosa: a clinicopathologic study of 268 cases. Carpenter WM. Prognostic factors in oral squamous cell carcinoma. Am J Otolaryngol 1999. Actinomycosis: a potential complication of head and neck surgery.34:239–46. Vann Oijen MG. Zitsch RP III. Oral Maxillofac Surg 1999. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2001. Recurrent aphthous ulcers: a review of diagnosis and treatment. Anticancer Res 1999. Oral Surg Oral Med Oral Pathol 1980. Rodolico V. Hansen L.37:164–74. Current concepts in oral cancer. Main JHP.49:139–47. Oral field cancerization: carcinogeninduced independent event or micrometastatic deposits? Cancer Epidemiol Biomarkers Prev 2000. The deep mycoses in HIV infection.19:3503–10. Pigmentary Disorders Barker B. Birek C. Scully C. Buchner A. J Am Dent Assoc 1996.66:59–61. Luciani A. Human papillomavirus as a risk factor for squamous cell carcinoma: a meta-analysis. Aust Dent J 1999. Savage NW. Miller CS. Daniels TE. Colby TV. Melkersson-Rosenthal syndrome and orofacial granulomatosis.3(Suppl 1):S200–7. Sugerman PB. Rogers RS III.
Superficial melanomas of the oral cavity. Regezi JA. Mucosal. Cancer 1985.48:61–4.14:448–65.11: 43–8.66:72–4. Lenane P. Gorsky M. Hodgson RP. Hayward J. Oral pigmentation.32:887–9.45:730–40. Dole EJ.106:582–7. Bilateral oral melanoacanthoma. Dermal melanocytosis: a clinical spectrum. Stanford DG. Koops MK. Heine RD II. Pickens T. . Prasad ML. Oral Surg Oral Med Oral Pathol 1987.37:19–25. et al. Ljungquist A. Forsell M. Oral presentation of minocyclineinduced black bone disease. Erickson QL. Pigmented nevi of the oral mucosa: a clinicopathologic study of 36 new cases and review of 155 cases from the literature. Drummond JF. Minocycline-associated tooth staining. Morency R. Georgouras KE.63:676–82.72:362–6. Mayo Clin Proc 1997. Fukuta Y. Eur J Oral Sci 1998. et al. Gen Dent 1996. Oral Surg Oral Med Oral Pathol 1998. Minocycline-induced staining of the tooth roots: a case report with histological and microanalytical studies. J Oral Sci 2001. Takeda Y. Ann Pharmacother 1998. and unusual clinical variants of melanoma. Expression of melanocytic differentiation markers in malignant melanomas of the oral and sinonasal mucosa. Gibson LE.44:451–2. Cutis 2000. Iversen K. Melanoma arising from the mucosal surfaces of the head and neck. Elston DM. Heine BT. Dental and oral discolorations associated with minocycline and other tetracycline analogs.354 PDQ ORAL DISEASE Buchner A. Falesky EJ. Oral Surg Oral Med Oral Pathol 1978. Greer RO. Hansen L.43:213–5. J Esthet Dent 1999. Odell EW. Oral pigmentation induced by Premarin. Rogers RS III. Perusse R. Goltz LE. Cutis 1991. Bennahum DA. Part II: analysis of 191 cases. genital. Cheek CC.86:715–9.79: 459–61. Primary malignant melanoma of the oral cavity: a review of 177 cases. Larsson B. Jungbluth AA.25:782–7. Fukuta Y. Damm DD. J Eur Acad Dermatol Venereol 2000. et al. Dodd MA. et al. Oral Surg Oral Med Oral Pathol 1995. Mercury content in amalgam tattoos of human oral mucosa and its relation to local tissue reactions. Heymann HO. Epstein JB. Troutman WG.55:1543–51. Am J Surg Pathol 2001. Australas J Dermatol 1996. Powell FC. Addison’s disease: the potentially life-threatening tan. Rapini RP. Haskell R.
Regauer S. Cribier B. Focal epithelial hyperplasia: a multifocal oral human papilloma virus infection. . Oral melanin pigmentation related to smoking in a Turkish population. Calobrisi SD. Paksoy C. Oral Oncol 1999. Van Den Eeden SK. Wallstrom M. Habel LA. Pediatr Dent 2000. Beham A. Shereman KJ. and electron-microscopic study.199:208–12. Chauvin PJ. Pyostomatitis vegetans associated with asymptomatic ulcerative colitis: a case report. Philpot NS. Beham-Schmid C. Nilsson F. et al. Chen SY. Verrucal-Papillary Lesions Batsakis JG. N Y State Dent J 1995. Sand L. Melanoma in situ of the oral mucosa in an adolescent with dysplastic nevus syndrome. McDonald JS. J Am Acad Dermatol 2000.48:62–4. Suarez P. Verveniotis SJ. Soykan E. Unsal E.29:272–7. Eversole LR.22:153–4. Grosshans E. Addiction 1999. Medical and surgical treatment. Miller AS. A populationbased study.79:452–4. el-Naggar AK. Chaudhry SI. Sex Transm Dis 1998. Asch P. Odell EW. Hirsch JM. Flaitz CM. Oral condyloma acuminatum. et al. Penna KJ. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1999. Differentiating squamous cell carcinoma from keratoacanthoma by histopathological criteria. J Oral Maxillofac Surg 1997. Pyostomatitis vegetans associated with ulcerative colitis. Soyer HP. et al. Risk factors for incident and recurrent condylomata acuminata in women. Adv Anat Pathol 1998. Gen Dent 2000. Brennan TD. The long-term effect of nicotine on the oral mucosa. Mutasim DF.28:922–7. O’Brien EA. Is it possible? A study of 296 cases.61:30–3. Lymphangiomatous macroglossia. J Calif Dent Assoc 2000.55:932–5. Papillary lesions of the oral cavity: relationship to human papillomaviruses.94:417–23.42(5 Pt 1):844–6. Temporary clearance with fluocinonide gel and complete remission after colectomy. immunohistochemical.25:285–92.35:354–9. Keratoacanthoma: a clinically distinct variant of well differentiated squamous cell carcinoma. Dermatology 1999.Additional Reading 355 Tremblay JF. Community Dent Oral Epidemiol 2001. Manganaro AM. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1995. Lymphangiomas of the oral cavity: a clinicopathologic.5:269–80. Proliferative verrucous leukoplakia and its related lesions.87:327–30.
Benign neural tumors of the oral cavity: a comparative immunohistochemical study. Branstetter BF. Tsuji T. Antoniades DZ. Intralesional corticosteroids injection for treatment of central giant-cell granuloma. immunohistochemical. Paticoff KA. Bergesio F. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1997. Dewitt D.132: 186–90. Molecular aspects of bone formation and bone growth. Merging the old skeletal biology with the new. Bandini S.9:472–6. J Am Dent Assoc 2001. Belazi M. J Craniofac Surg 1998. Connective Tissue Lesions Adornato MC. J Nephrol 2001. Fowler CB. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2000. Benign fibro-osseous lesions: a review of current concepts. Chen SY. Osteogenic sarcoma of the jaws: factors influencing prognosis.32:1–21. Chrysomali E.90: 731–8. J Craniofac Genet Dev Biol 2000. Regezi JA. Verrucous carcinoma.84:381–90. Dekker NP. Conti P. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1998. Concurrence of torus palatinus with palatal and buccal exostosis: case report and review of the literature.8:126–43.26:198–204. Papanicolaou SI. J Am Acad Dermatol 1995. Brennan D. Cascone P. Barrett AW. Progressive systemic sclerosis: rare localization of the maxillofacial district. . August M. Superficial arteriovenous hemangioma of the oral cavity.85:552–7. Nodular macroglossia with combined light chain and beta-2 microglobulin deposition in a long-term dialysis patient. Brannon RB.20:587–9. Am J Surg 1998. J Cutan Pathol 1997. Weissman JL. Kaplan SB. Adv Anat Pathol 2001.176:393–7. Int J Oral Maxillofac Surg 1997.20:94–106. et al. Lymphangiomas of the oral cavity: a clinicopathologic.356 PDQ ORAL DISEASE Schwartz RA. Magennis P. Verrucous carcinoma of the skin and mucosa.55:932–5. Speight PM. Cohen MM Jr. Spiro RH. J Oral Maxillofac Surg 1997. Am J Neuroradiol 1999. and electron-microscopic study. then and now. Papanayiotou P.14:128–31. Vetrano S. Keratoacanthoma and squamous cell carcinoma: study of PCNA and Le(Y) expression. Miller AS. Imaging of a Stafne bone cavity: what MR adds and why a new name is needed.24:409–15. II. Rivaroli A.
Otolaryngol Head Neck Surg 2001. Bone sarcomas of the head and neck in children: the St Jude Children’s Research Hospital experience. Daw NC. Shore T. radiographic evaluation and treatment analysis of 17 cases. van den Akker HP. Loewen R.88:2172–80. Hornstein OP. Aneurysmal bone cysts of the jaws: clinicopathological features.124:164–9.66:78–9. Larsen P. J Can Dent Assoc 2000. Destructive membranous periodontal disease (Ligneous periodontitis). Gingival hyperplasia complicating acute myelomonocytic leukemia. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2000. Bernstein CN. Epivatianos A. Benign tumors of adipose tissue of the oral cavity: a clinicopathologic study of 13 cases. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2000. Periapical central giant cell granuloma: a potential endodontic misdiagnosis. .3:31–8. J Periodontol 1999.58:1113–7. Horn C. Cancer 2000.70: 919–25. Leao JC. et al. 19:75–9. Tampakopoulou DA. Warrington R. Dahlkemper P. Markopoulos AK.13: 152–4. Tsai CC. Kalantar Motamedi MH. Meyer WH. Hicks ML. et al. Gunhan O. Hou GL. Oral Dis 1997. Scully C. J Dermatol 1997. Anomalies of craniofacial skeleton and teeth in cleidocranial dysplasia. Keratinocyte growth factor is upregulated by the hyperplasia-inducing drug nifedipine. Tongue lesions in the pediatric population.26:56–62. Thaker HM. et al. Rosenberg AJ. Kreiborg S. et al.90: 694–704. De Lange J. Papanayotou P. Jensen BL. Mahmoud HH. Huang JS. Porter S. Analysis of oral manifestations of leukemia: a retrospective study. Ilnyckyj A. J Oral Maxillofac Surg 2000. Can J Gastroenterol 1999. Pringle GA. Treatment of giant cell granuloma of the jaw with calcitonin. Berker E. J Craniofac Genet Dev Biol 1999. Crohn’s disease and the Melkersson-Rosenthal syndrome. Aldor TA. Human herpesvirus 8 and oral health care: an update. et al.24:281–96.28:372–6. Int J Oral Maxillofac Surg 1999. Olsen I. Melkersson-Rosenthal syndrome—a challenge for dermatologists to participate in the field of oral medicine.12:1566–9.Additional Reading 357 Cooper CL. Das SJ.90:739–45. Wolcott JF. Cytokine 2000. Gunhan M. J Craniomaxillofac Surg 1998.
Grace MG.65:158–66. Melkersson-Rosenthal syndrome and orofacial granulomatosis. The gene for cherubism maps to chromosome 4p16. Maxillofacial fibro-osseous lesions: classification and differential diagnosis. Said-Al-Naief N.13:104–12. Robinson PA. Perniciaro C. Hume WJ. J Oral Pathol Med 1996. Orofacial radiological manifestations of systemic sclerosis.21:1283–309. Potts AJ. Rout PG.25: 163–9. Tiziani V. Dermatol Clin 1996. Gardner’s syndrome. Ann Diagn Pathol 2001. et al. Hamburger J.16:328–36. Ogawa I. Oral spindle cell lipoma. Takata T. Mighell AJ. Reichenberg E. Bekic M. Blake M. Paget’s disease of bone: diagnosis and treatment update. Semin Diagn Pathol 1996. Rogers RS III. Radiographics 2001.80:744–50. Diseases of the lips. Sciubba JJ. Dermatol Clin 1995. Rodan GA.5:207–15.358 PDQ ORAL DISEASE McNamara CM. Ueki Y. Nat Genet 2001. Petrikowski CG. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1995. Meraw SJ. Cleidocranial dysplasia: radiological appearances on dental panoramic radiography. Curr Rheumatol Rep 2000. et al. Sheridan PJ. Miyauchi M. Noor M.28:125–6. Osteosarcoma of bone. Slootweg PJ. Buzzo CL.28:89–97. J Oral Pathol Med 1995. Imaging of giant cell tumor and giant cell reparative granuloma of bone: radiologic-pathologic correlation. .24:285–7. Am J Hum Genet 1999.2:67–73. Murphey MD. Santanna C. Mayo Clin Proc 1998. Flemming DJ.289:1508–14. Semin Cutan Med Surg 1997.13:51–6. O’Riordan BC.73:1196–9. Tiziani V. Sandy JR. Shoback D. Unni KK. Pharoah MJ. J Orthop Sci 1998. Science 2000. Radiographic differentiation of osteogenic sarcoma. Dentomaxillofac Radiol 1996. Martin TJ. et al. Mutations in the gene encoding c-Ablbinding protein SH3BP2 cause cherubism. et al. Nomikos GC. Medically induced gingival hyperplasia. Lee L. Zahurullah FR. Rogers RS III.14:371–9. Therapeutic approaches to bone diseases. Dentomaxillofac Radiol 1999.3:287–94.25:193–6. Florid cemento-osseous dysplasia with concomitant simple bone cysts: a case in a Japanese woman. osteomyelitis and fibrous dysplasia of the jaws. Immunolocalisation of tenascin-C in focal reactive overgrowth of oral mucosa.
Cardoso SV. Crit Rev Oral Biol Med 2001. J Acquir Immune Defic Syndr 1999.61:6–10. Fox RI. Esch TR. differential diagnosis.111:89–95. Possible involvement of EBV-mediated alpha-fodrin cleavage for organ-specific autoantigen in Sjogren’s syndrome.9:2007–16. Acta Haematol 2001. Bachrach SJ. J Rheumatol Suppl 2000.154:1214–8. Nakayama E. Arch Pediatr Adolesc Med 2000. et al. Lakin RC. Yuwono M. Mucus extravasation phenomenon in newborn babies: report of two cases. Ono M. Sato M. Potulska A. Mier RJ. Yuasa K. Evaluation. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1998. Inoue H. Tjota A. Yarchoan R. and treatment of xerostomia. Int Arch Allergy Immunol 1996. Dorfman HD.28:30–3. Loyola AM. J Oral Pathol Med 1998.105:83–8. et al. Tsubota K.7:329–32. Moreti MM. Fisher JE. et al. Sjogren’s syndrome: current therapies remain inadequate for a common disease. Rossi TM. Salivary Gland Diseases Biasi D.166:3801–9. Expert Opin Investig Drugs 2000.11:74–7. Significant correlation between matrix metalloproteinase activity and tumor necrosis factor-alpha in salivary extravasation mucoceles. Azuma M. Quantitative assessment of parkinsonian sialorrhea and results of treatment with botulinum toxin. Hoque MO.28:350–3. . Imaging findings of some buccomasseteric masses. Yonetsu K.12:244–51. Int J Paediatr Dent 2001. Treatment of sialorrhea with glycopyrrolate: a double-blind. Daniels TE. Oncogene expression in patients with familial polyposis coli/Gardner’s syndrome. Parkinsonism Relat Disord 2001.86:755–9. Mucosa-associated lymphoid tissue lymphoma of the salivary glands occurring in patients affected by Sjogren’s syndrome: report of 6 cases. Therapy for Kaposi’s sarcoma: recent advances and experimental approaches. dose ranging study. Ambrosetti A. Friedman A. Gatti AF. Skeletal Radiol 1999. et al. Caramaschi P. Pathogenetic factors in Sjogren’s syndrome: recent developments. Eisig S. Cherubism: clinicopathologic features. J Immunol 2001.21 Suppl 1:S66–73.Additional Reading 359 Yamaguchi T.
Savage NW. Experimental study on necrotizing sialometaplasia of the palate. chemotherapy. Kanis JA. Niedobitek G. Radiographic manifestations of multiple myeloma in the mandible. Shigematsu Y. Primary non-Hodgkin’s lymphoma of the mandible treated with radiotherapy. Ohgi K. Epstein-Barr virus: biology and disease. A retrospective study of 77 patients. . De Marco L.25:229–41. et al. Bagan JV. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2000. Shigematsu H. Nocini P. Williams DM. Noguchi Y. Cysts Aguilo L. Outcomes of submandibular duct re-implantation for sialorrhea.88(12 Suppl):3022–32. et al.27:44–7. Hansen LS. Porter S. Klein K. Bisphosphonates in multiple myeloma. et al.83:265–71. Orofacial disease: update for the dental clinical team: 11. Neumann HJ.58:636–44. J Oral Maxillofac Surg 2000. Fujita K.26:143–6. Chen SY. Cervical lymphadenopathy.360 PDQ ORAL DISEASE Panarese A. Sugerman PB. Int J Oral Maxillofac Surg 1996. Oral Surg Oral Med Oral Pathol 1980. Lymphoid Lesions Buchner A.30:125–8. A clinicopathologic study of thirty-eight cases. Hodgson D. Shimooka H. Pisano JJ. Borges AC.90:478–82. Gandia JL. Role of local anesthetic injections. Witt C. Oral Dis 1997.65:102–6.90:450–5. Castro WH. Barreto DC. Lo Muzio L. J Oral Pathol Med 2001. Cibrian R. Fior A. Plasmacytoma of the oral cavity and jaws: a clinicopathologic study of 13 cases. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2000.55:450–3. J Oral Maxillofac Surg 1997. Lymphoepithelial cysts of the oral cavity. Coupland R. McCloskey EV. Cruchley AT. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1997. Primary non-Hodgkin’s lymphoma of the jaws: immunohistochemical and genetic review of 10 cases. ASDC J Dent Child 1998. and autologous peripheral blood stem cell transplantation. Glandular odontogenic cyst: absence of PTCH gene mutation. Dent Update 2000. Miller AS.3 Suppl 1:S156–63. Cancer 2000. Mucocele of the anterior lingual salivary (glands of Blandin and Nuhn): report of 5 cases. Scully C.50:441–9. Ghosh S. Gomez RS. Young LS. Kirita T. Eruption cysts: retrospective clinical study of 36 cases. Clin Otolaryngol 2001. Young WG.
Semin Diagn Pathol 1999. Cunningham MJ. Meara JG. Nevoid basal cell carcinoma syndrome. Tumors and cysts of the jaws. Edmondson HD. Mathews J. Clinical manifestations in 105 persons with nevoid basal cell carcinoma syndrome. Oxford: Wright. Carney YL. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1995. Calcifying odontogenic cyst—a characteristic CT finding. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1996. Fantasia JE. Lancaster J. Altini M. Glandular odontogenic cysts. Shear M. Rubini C.16: 288–92. Kimonis VE. Gorlin RJ.28:216–23.35:196–8. Odontogenic ghost cell tumor. et al. Browne RM. Roman S. Ellis GL. clinical significance and diagnosis. J Laryngol Otol 2001. J Oral Maxillofac Surg 2000. Congenital cysts and fistulas of the neck. Differentiation of odontogenic keratocysts from other odontogenic cysts by the expression of bcl-2 immunoreactivity. Rushton VE. The lateral periodontal cyst: aetiology.50:787–91.115:333–5. Oral Oncol 1998. . Sciubba JJ.79:593–602. Unicystic ameloblastoma. Philipsen HP. Horner K. Diagnosis and treatment.Additional Reading 361 Carter LC. Nicollas R. Kerezoudis NP. Ali H. Traumatic bone cysts in the jaws of a Hong Kong Chinese population. Siskos G. Cysts of the oral regions.34:404–7. Kahn LB. Nevoid basal cell carcinoma syndrome: molecular biology and new hypotheses. Fioroni M. et al. Pastakia B. Perez-Pudlewski D. Lateral periodontal cyst. O’Sullivan G. Hussain K. Cytokeratin expression in the odontogenic keratocyst.38:312–7. True lateral dermoid cyst of the floor of the mouth. Clin Radiol 1995.69:299–308. Am J Med Genet 1997. Shah SS.34:317–25. Piattelli A.55:117–24. 2001. Triglia JM. 1992.16:144–50. Int J Oral Maxillofac Surg 1999. Oral Oncol 1998. MacDonald-Jankowski DS. Use of calretinin in the differential diagnosis of unicystic ameloblastomas. Guelfucci B. Pilch BZ. A review of 193 cases from the literature. Reichart PA. Multifactorial analysis of a previously unreported series. Coleman H. Cohen MM Jr. Endod Dent Traumatol 2000. 13:113–25. Goldstein AM. Donta-Bakoyianni C. Int J Pediatr Otorhinolaryngol 2000.58:862–6. Washington: Armed Forces Institute of Pathology.81:210–6. Dermatol Clin 1995. Br J Oral Maxillofac Surg 1997. Histopathology 2001.
Pilkington RJ.83:577–83. Dominguez FV. Naor H. Teratomas. Kaffe I. Ameloblastoma: a clinical. Odontogenic Tumors Barker BF. High AS. dermoids. Desmoplastic and non-desmoplastic ameloblastoma: a comparison clinicopathological analysis. Oral Dis 1999. Paparella ML. Value of computed tomography and magnetic resonance imaging in the treatment of a calcifying epithelial odontogenic (Pindborg) tumour. Ki-67 antigen and protein in epithelium of glandular odontogenic cysts and dentigerous cysts. radiographic. Robinson PA. Extraosseous calcifying epithelial odontogenic tumor: report of two cases and review of the literature.194:473–7. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2001. Kim SG. Kapranos N. Retrospective analysis of 31 cases of nasopalatine duct cyst. Radiographics 1995.30:14–25. Houston GD.29:139–44. et al. Vasconcelos R. Markham AF. Zedan W.15:1437–55. Chiechi MV.16:297–301. Antoun NM. A radiologic analysis of dentigerous cysts and odontogenic keratocysts associated with a mandibular third molar. Tsukamoto G.27:49–52. Keszler A.38:154–7.362 PDQ ORAL DISEASE Smirniotopoulos JG. Immunohistochemical study of bcl-2 protein.26:299–303. Toida M. Int J Oral Maxillofac Surg 2001. Odontogenic myxoma.5:325–8.2:228–31. Semin Diagn Pathol 1999. and histopathologic analysis of 71 cases. J Oral Pathol Med 2000. Expression of the Sonic Hedgehog receptor “PATCHED” in basal cell carcinomas odontogenic keratocysts. Br J Oral Maxillofac Surg 2000. and epidermoids of the head and neck. . et al. de Aguiar MF. Kakarantza-Angelopoulou E. Adlam DM. Odontogenic fibroma. Dentomaxillofac Radiol 1997. Stoelinga PJ.91:649–53. J Pathol 2001. Cross JJ. Sasaki A. Long-term follow-up on keratocysts treated according to a definite protocol. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1997. Tosios KI. So-called calcifying odontogenic cyst: review and discussion on the terminology and classification. Castro W. J Oral Pathol Med 1998. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2001. Semin Diagn Pathol 1999. Akiyama T. Buchner A. Clinical and radiological features of odontogenic myxoma of the jaws. Oral Dis 1996. Dunlap CL.91:743–7. Jang HS. Fowler CB.16:293–6.
Takata T. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1996. Management of mandibular ameloblastoma: the clinical basis of a treatment algorithm.82:426–33. Manor Y.19:139–42.36:17–26.33:86–99. Ng KH. Praetorius F. immunohistochemical.21:261–4.37: 455–60. et al. Oral Oncol 1999. Philipsen HP. Reichart PA.57: 1074–7. Cetingul E. Nocini P. Favia G. Ameloblastic fibroma and related lesions: current pathologic concept. Lo Muzio L. Adenomatoid odontogenic tumour: facts and figures. radiologic. Oral Oncol 1997. Taicher S. and ultrastructural study. Reichart PA.35:125–31. J Clin Pediatr Dent 1997. Dental odontomas: a retrospective study of 104 cases. Semin Diagn Pathol 1999. Unusual peripheral odontogenic tumors in the differential diagnosis of gingival swellings. Gunbay T. et al. Merdinger O. Katz J. Mincer HH.Additional Reading 363 Li TJ. Tomich CE.24:1385–92. Calcifying epithelial odontogenic tumour: biological profile based on 181 cases from the literature. J Clin Periodontol 1999. Philipsen HP.35:535–40. discussion 1078–9.38:19–22. Considerations on interrelationship. Philipsen HP. Biological profile based on 100 cases from the literature and own files. Unal T. Oral Oncol 2001. Wu YT. Takeda Y. Reichart PA. Philipsen HP. Yu SF. Siar CH. Br J Oral Maxillofac Surg 2000. Odontogenic myxoma of the jaws: a clinical. Yu GY. Desmoplastic ameloblastoma (including “hybrid” lesion of ameloblastoma). review of the literature and presentation of new cases of odontomas. Oral Oncol 2000. Sampson DE. .26:806–9. Unicystic ameloblastoma: a clinicopathologic study of 33 Chinese patients. J Oral Maxillofac Surg 1999. Owens BM. Clinicopathological study of peripheral odontogenic fibromas (WHO-type) in Malaysians (1967–95). Schuman NJ. Oral Oncol 1999. Benign mixed odontogenic tumors. J Clin Pediatr Dent 1995. Mixed odontogenic tumours and odontomas. 16:308–16. Am J Surg Pathol 2000. Reichart PA. Pogrel MA. Peripheral adenomatoid odontogenic tumor: birth of a term.
Langerhans’ cell histiocytosis: paediatric head and neck study. Jainkittivong A.15:237–42. II. Cohen ME. and evidence for buttressing bone formation. Surgical management of carotid body tumors. Dentomaxillofac Radiol 1998. Hostette R. Speight PM. Su L. Barauskas TM. Weathers DR.123:202–6. Wang MB.29:649–53. Addy M. A clinical and radiologic study of 316 cases. MacDonald-Jankowski DS. J Oral Pathol Med 2000. Bond M.364 PDQ ORAL DISEASE Benign Nonodontogenic Tumors Al-Ammar AY.84:540–9. Ann Vasc Surg 2001.29:13–8.28: 266–72. An analysis of eight cases and a comparison with other fibro-osseous lesions. Weathers DR. Saunders JG. Buccal alveolar exostoses: prevalence. Bell CN. Paragangliomas—a decade of clinical experience. Calcaterra TC. Distinguishing features of focal cemento-osseous dysplasia and cemento-ossifying fibromas. Horning GM. Freischlag JA.25:340–2. .10:442–6. Williams HK. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1997. Mangham C. Kohn JS. A pathologic spectrum of 316 cases. Langerhans cell histiocytosis presenting as bilateral eosinophilic granulomata in the molar region of the mandible. Waldron CA. Kafie FE. Familial carotid body tumors: a closer look. J Craniofac Surg 1999. Neils TA. Su L. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2000. Holmes AD. Krouse R. Waldron CA. Jewell ER. Radden BG. Schloss MD. J Clin Periodontol 1998. Wang SJ. Distinguishing features of focal cemento-osseous dysplasias and cemento-ossifying fibromas: I. Eveson JW. Tewfik TL. Langlais RP.90:48–53. Somasunder P.27:298–304. Heggie AA. Raftery KB. Juvenile ossifying fibroma. characteristics. J Periodontol 2000.84:301–9. Juvenile ossifying fibroma of the midface. et al. J Surg Oncol 2000. Carotid body tumors: the role of preoperative embolization. Otolaryngol Head Neck Surg 2000. Shand JM. Buccal and palatal exostoses: prevalence and concurrence with increasing age.71:1032–42. A case report. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1997.10:442–6. Cemento-ossifying fibromas in the jaws of Hong Kong Chinese. J Vasc Surg 1999. J Otolaryngol 1999.
Head Neck 1998. Bras J. Groot RH. Eyrich GK.72:461–9. Papanagiotou P. Boulinguez S. Pajarola G.20:411–7. Antoniades D. van den Akker HP. Virolainen E. Sinusitis as the first indication of sarcoidosis an incidental finding in a patient with presumed ‘odontogenic’ sinusitis: case report. Reix S. Oral manifestations of sarcoidosis. J Can Dent Assoc 2001. Adjunctive hyperbaric oxygen in irradiated patients requiring dental extractions: outcomes and complications.38:277–9. Sandor GK. Hyperbaric oxygen therapy and mandibular osteoradionecrosis: a retrospective study and analysis of treatment outcomes. Kolokotronis A. Cyclooxygenase-2 is upregulated in inflamed gingival tissues. Adkinson CD. Oral Dis 1997. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2000. et al. J Oral Maxillofac Surg 2001. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1997. Yahatom R. Granulomatous cheilitis: a study of six cases. Tumor necrosis factoralpha and transforming growth factor-beta 1 in chronic periapical lesions. A modified protocol for early treatment of osteomyelitis and osteoradionecrosis of the mandible. Primary chronic osteomyelitis associated with synovitis. van Merkesteyn JP. J Oral Pathol Med 1999. Br J Dermatol 2000. Oral Oncol 1998. Taicher S. pustulosis. Diffuse sclerosing osteomyelitis and florid osseous dysplasia. Ramachandran Nair PN. Role of drug exposure in aphthous ulcers: a case-control study. Oral ulceration as a presenting sign of unknown sarcoidosis mimicking a tumour: report of 2 cases. Di Alberti L. Linder LE. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1996. J Periodontol 2001. Morton RS. Trigonidis G. . Blinder D.59:518–22. Danin J. Evans AW.67:384. Harder C.Additional Reading 365 Inflammatory Diseases Aitasalo K.143:1261–5.3:188–92. Niinikoski J. hyperostosis and osteitis (SAPHO syndrome). Types and incidence of human periapical lesions obtained with extracted teeth. 90:514–7. Lindeboom JA. Andersson L. David LA. Lundqvist G. Grenman R. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1996. Schroeder HE. Bedane C.83:458–61. Piattelli A. et al.28:456–64. Br J Oral Maxillofac Surg 2000. Dongari-Bagtzoglou AI.81:93–102. Chavez JA. Sailer HF. Brown DH.81:333–42.34:427–30. Favia GF. acne.
Conway KR. ASDC J Dent Child 1997. Kurisu K. Smith BG. Brenneise CV. Lee IW.87:752–5.23:158–62. type II: report of 2 new families and review of the literature. et al. The relationship between gastrooesophageal reflux disease and dental erosion. The aetiology and clinical appearance of tooth wear. Osteosarcoma of the jaws: a 30-year retrospective review. Torriani DD. . Crawford PJ. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1999. Tabata MJ. Dentinal dysplasia type I: review of the literature and report of a family. Colquhoun AN. Bishop K. Numb chin syndrome in Ewing sarcoma. Oral Oncol 2000. Ayers KM. Osteogenic sarcoma of the jaws: factors influencing prognosis.3:223–8. Antunes NL. Dewitt D.64:46–8. Boer FA. Ahn SK.36:27–31. Gorsky M.26:198–204. J Pediatr Hematol Oncol 2000. Cunha RF.22:521–3. Ciba Found Symp 1997. Pardo J. J Oral Maxillofac Surg 1990. Bennett JH. Thomas G. Eur J Prosthodont Restor Dent 1997. Lee SH. Oral Dis 1997. Anavi Y. Lara JR. Pediatr Dent 2001. neck. Zaizov R. Ewing tumor: tumor biology and clinical applications. J Oral Rehabil 1996. 23:289–97.366 PDQ ORAL DISEASE Tooth Abnormalities Aldred MJ. Kelleher M. Ansari G. Kaplinsky C. Epstein JB. August M. Leukaemia in children. Cutis 1999. Natal and neonatal teeth: review of the literature. Lis E. Gorlick R. Speight PM. Evans DF.205:200–5. Human genes for dental anomalies. Part I: Orofacial complications and side-effects of treatment. Kowalski LP.90:323–32.96:60–5. N Z Dent J 2000. Bartlett DW. Craniofacial osseous and chondromatous sarcomas in British Columbia—a review of 34 cases.48:708–13. Head Neck 2000. Magennis P. Choi EH. Dentin dysplasia. de Alava E.22:207–14. Callaja E. Int J Surg Pathol 2001. Frossard WT. Bagietto R. Molecular biology of hereditary enamel defects. Prognostic significance of the distribution of neck node metastasis from oral carcinoma. Evans AW. Reid JS.9:7–17. and maxillofacial childhood Burkitt’s lymphoma: a retrospective analysis of 31 patients. Int J Oral Maxillofac Surg 1997. Head. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2000.64:429–34. Calderon S. Leukemic macrocheilia associated with chronic lymphocytic leukemia.5:157–60.
Pediatr Dent 2000. J Oral Maxillofac Surg 1997.22:207–14. Bouquot JE. et al. Newman HN. Minnesota. Cancer 2000. Prognostic significance of the distribution of neck node metastasis from oral carcinoma. Pisano JJ. Callaja E.90:323–32. Bone sarcomas of the head and neck in children: the St Jude Children’s Research Hospital experience. de Alava E.55:450–3. Investigation and treatment of patients with teeth affected by tooth substance loss: a review. Burke FJ. Kurland. Risk factors for dental fluorosis: a review of the recent literature. Mahmoud HH. Osteogenic sarcoma of the jaws: factors influencing prognosis. Rozier RG. Pardo J. Gorsky M. Etiology of dental erosion-intrinsic factors. . and the periodontium. Weiland LH.11:212–8. Daw NC.9:7–17. Miller AS. Chen SY. Coupland R. Plasmacytoma of the oral cavity and jaws: a clinicopathologic study of 13 cases. Oral Oncol 2000. Attrition. Dewitt D. Int J Surg Pathol 2001. eruption. Head Neck 1989. Meyer WH. Evans AW. Scheutzel P. et al.36:27–31. Magennis P. The prevalence and severity of enamel fluorosis in North American children. Craniofacial osseous and chondromatous sarcomas in British Columbia—a review of 34 cases.88:2172–80. Int J Oral Maxillofac Surg 1997.22:269–77. J Dent Res 1999.104(2 Pt 2):178–90. Metastases to and from the upper aero-digestive tract in the population of Rochester. Watson ML. Lara JR.78:730–4.22:521–3. Neumann HJ. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2000. Bennett JH. Witt C. Malignant Nonodontogenic Tumors Antunes NL. J Public Health Dent 1999.Additional Reading 367 Mascarenhas AK. Radiographic manifestations of multiple myeloma in the mandible: a retrospective study of 77 patients.83:265–71.26:198–204. Ewing tumor: tumor biology and clinical applications. Llein K. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1997. Numb chin syndrome in Ewing sarcoma. August M. Thomas G. Epstein JB.discussion 454–5. Head Neck 2000.59:239–46. 1935–1984. Speight PM. Borges AC. Osteosarcoma of the jaws: a 30-year retrospective review. Kowalski LP. Gorlick R.27:175–83. Eur J Oral Sci 1996. J Pediatr Hematol Oncol 2000. Lis E. Bagietto R. Dent Update 2000.
17:283–90. Surgical management of macroglossia due to primary amyloidosis.28:129–31. Metabolic and Genetic Disorders Bilezikian JP. Relationship between periodontal disease and systemic health.25:21–36. Danesh F. Int J Oral Maxillofac Surg 1999. J Craniomaxillofac Surg 1989.1:237–45. Taicher S. Ho LT. Krall EA. Mardinger O.1:297–305. Dialysis-related amyloidosis: history and clinical manifestations. Rev Endocr Metab Disord 2000. Hoffman C. Hendy GN. jaws and surrounding tissues. Henshaw MM. Rev Endocr Metab Disord 2000. Chaushu G. Silverberg SJ. Rotenberg L. Neoplasms metastatic to the mouth. Meisher I. Garcia RI.3:287–94.5:101–4.14:80–5. J Cutan Med Surg 2001. Clinical spectrum of primary hyperparathyroidism. Zachariades N. Goldstein AE. Kakani RS. Molecular mechanisms of primary hyperparathyroiodism. . Osteosarcoma of bone. Periodontol 2000 2001.368 PDQ ORAL DISEASE Unni KK. J Orthop Sci 1998. Semin Dial 2001. Nodular amyloidosis: case report and literature review.